Increased (ICP) Intracranial Pressure o Increased concentration of carbon

dioxide will cause VASODILATION à

 Intracranial pressure more than 15 mmHg
 Brunner= Normal intracranial pressure 10-20 increased flowà increased ICP
mmHg
 Monro-Kellie hypothesis: because of limited  Cerebral Edema
space in the skull, an increase in any one skull
o Abnormal accumulation of fluid in the
component—brain tissue, blood, or CSF—will
intracellular space, extracellular space
cause a change in the volume of the others
or both.
 Compensation to maintain a normal ICP of 10
o Edema can occur in gray, white or
to 20 mm Hg is normally accomplished by
interstitial matter.
shifting or displacing CSF
 Herniation
 With disease or injury, ICP may increase
• Results from an excessive increase in
 Increased ICP decreases cerebral perfusion,
ICP when the pressure builds up and
causes ischemia, cell death, and (further)
the brain tissue presses down on the
edema
brain stem
 Brain tissues may shift through the dura and
 Cerebral response to increased ICP
result in herniation
• The brain can maintain a steady
 Autoregulation: refers to the brain’s ability to perfusion pressure if the arterial
change the diameter of blood vessels to systolic blood pressure is 50 to 150
maintain cerebral blood flow during alterations mm Hg and the ICP is less than 40 mm
in the systemic blood pressure Hg

 CO2 plays a role; decreased CO2 results in
vasoconstriction, and increased CO2 results in
vasodilatation
 Pathophysiology
• The cranium only contains the brain
substance, the CSF and the blood/blood
vessels
• MONRO-KELLIE hypothesis- an increase in
any one of the components causes a
change in the volume of the other
• Any increase or alteration in these structures
will cause increased ICP
• Increased ICP from any cause decreases
cerebral perfusion, stimulates further
swelling(edema, and may shift brain tissue
through openings in the rigid dura,
resulting in hernation, a dire and a
frequently fatal event
Compensatory mechanisms:
 1. Increased CSF absorption
 2. Blood shunting
 3. Decreased CSF production
Decompensatory mechanisms:
 1. Decreased cerebral perfusion
 2. Decreased PO2 leading to brain
hypoxia
 3. Cerebral edema
 4. Brain herniation
 Decreased cerebral blood flow
o Increased ICP significantly reduce
cerebral blood flow, resulting in
ischemia and cell death
o Vasomotor reflexes are stimulated
initiallyà systemic pressure rises to
maintain cerebral blood flow à slow
bounding pulses and respiratory
irregularities
• Cushing’s response- is seen when
cerebral blood flow decreases
significantly. When ischemic →
vasomotor center triggers an increase
in arterial pressure in an effort to
overcome the increased ICP
• Vasomotor center triggers rise in BP to
increase ICP
• Sympathetic response is increased BP
but the heart rate is SLOW
• Respiration becomes SLOW
• CCP (cerebral perfusion pressure) is
closely linked to ICP
• CCP = MAP (mean arterial pressure) –
ICP
• Normal CCP is 70 to 100
• A CCP of less than 50 results in
permanent neuralgic damage
 Manifestations of Increased ICP—Early
o Changes in level of consciousness
o Abnormal respiratory and vasomotor
response
o Any change in condition
o Restlessness, confusion, increasing
drowsiness, increased respiratory
effort, and purposeless movements has
neurologic significance
o Stuporous, reactive only to loud and
painful stimuli (serious stage of brain
circulation is probably taking place)
 o Pupillary changes and impaired ocular o Evaluate neurologic status as
movements(Pupillary changes- fixed, completely as possible
slowed response)
o Glasgow Coma Scale
o Weakness in one extremity or one side
o Pupil checks
o Headache: constant, increasing in
intensity, or aggravated by movement o Assess selected cranial nerves
or straining
o Take frequent vital signs
o Vomiting
o Assess intracranial pressure
o Comatose and abnormal motor
response in the form of decortication o Nursing interventions:
(abnormal flexion of the upper
o Maintain patent airway
extremities and extension of the lower
extremities), decerbration (extreme
extension of the upper and lower  1. Elevate the head of the
extremities) of flaccidity bed 15-30 degrees- to
promote venous drainage
 Manifestations of Increased ICP—Late
 2. assists in administering
o Respiratory and vasomotor changes 100% oxygen or controlled
hyperventilation- to reduce
o VS: increase in systolic blood pressure, the CO2 blood
widening of pulse pressure, and levelsàconstricts blood
slowing of the heart rate; pulse may vesselsàreduces edema
fluctuate rapidly from tachycardia to
bradycardia and temperature increase  3. Administer prescribed
medications- usually
 Cushing’s triad: bradycardia,
hypertension, and bradypnea •Mannitol- to produce
negative fluid balance
o Projectile vomiting
•corticosteroid- to reduce
o Hyperthermia
edema
o Abnormal posturing
•anticonvulsants-p to
prevent seizures

 4. Reduce environmental
 Complications
stimuli
o Brain stem herniation: results from an
 5. Avoid activities that can
excessive increase in ICP in which the
increase ICP like valsalva,
pressure builds in the cranial vault and
coughing, shivering, and
the brain tissue presses down on the
vigorous suctioning
brain stem. Results in cessation of
blood flow to the brain, leading to
 6. Keep head on a neutral
irreversible brain anoxia and brain
position. ACOID- extreme
death.
flexion, valsalva
o Diabetes Insipidus: results of
 7. monitor for secondary
decreased secretion of ADH
complications
s/symp: excessive urine
•Diabetes insipidus- output
output, decreased urine
of >200 mL/hr
osmolality and serum
hyperosmolality
•SIADH
o SIADH: is the result of
increased secretion of ADH. Pt.  Medical Management:
becomes vol. overloaded, urine output
o Monitoring Intracranial Pressure and
diminishes, and serum sodium
concentration becomes dilute. Cerebral Oxygenation:
 Ventriculostomy: a fine-bore catheter is
inserted into a lateral ventricle,
preferably in the non dominant
o Nursing Process—Assessment of the Patient hemisphere of the brain.
With Increased Intracranial Pressure Use to drain blood from the ventricle.
Continuous drainage of CSF under
o Conduct frequent and ongoing pressure control is an effective method
neurologic assessment of treating intracranial hypertension.
 Subarachnoid screw or bolt: is a hollow
device that is inserted through the skull
 and dura mater into the cranial
subarachnoid space. Attached to the
pressure transducer and the output is
recorded on an oscilloscope.
 Epidural monitor: uses a pneumatic flow
sensor and functions without electricity.
Disadvantage: inability to withdraw CSF
for analysis
 Fiberoptic monitor: or transducer-tipped
catheter is an alternative standard
intraventricular, subarachnoid and
subdural system.
o Decreasing Cerebral Edema
 Osmotic diuretics: such as mannitol may
be administered to dehydrate the brain
tissue and reduce cerebral edema. Act by
drawing water across intact membranes,
thereby reducing the volume of the brain
and extracellular fluid.
 If brain tumor is the caused of the
increased ICP, corticosteroids
(dexamethasone) help reduce the edema
surrounding the tumor.
 Limiting overall fluid intake leads to
dehydration and hemoconcentration,
which draws fluid across the osmotic
gradient and decreases cerebral edema.
 Lowering body temperature would
decrease cerebral edema by reducing
the oxygen and metabolic requirements
of the brain, thus protecting the brain
from continued ischemia.
o Maintaining Cerebral Perfusion
 Cardiac output is made using fluid
volume and inotropic agents such as
dobutamine hydrochloride (Dobutrex)
and norepinephrine bitartate (Levophed).
The effectiveness of the cardiac output is
reflected in the CCP, which is maintained
at greater than 70 mm Hg.
o Reducing Cerebrospinal Fluid and
Intracranial Blood Volume
 CSF drainage is frequently performed,
because the removal of CSF with a
ventriculostomy drain can dramatically
reduce the ICP and restore CCP.
o Controlling Fever
 Fever increases cerebral metabolism
and the rate at which cerebral edema
forms.
 Administration of antipyretic
medications and use of hypothermia
blanket
o Maintaining Oxygenation
o Reducing Metabolic Demands
 Cellular metabolic demands may be
reduced through the administration of
high doses of barbiturates if the pt. is
unresponsive to conventional tx.
Barbiturates decrease ICP and protect
the brain is uncertain; administration of
pharmacologic paralyzing agents such
as propofol (Diprivan)
Cerebrovascular Accident/ ischemic stroke/ brain
attack
 Sudden loss of function resulting from
disruption of the blood supply to a part of the
brain.
 Different types of stroke based on the caused
o Large artery thrombotic stroke: caused by
artherosclerosic plaques in the large blood
vessels of the brain. Thrombus formation
and occlusion at site of the artherosclerosis
result in ischemia and infarction.
o Small penetrating artery thrombotic stroke:
also called lacunar stroke because of the
cavity that is created after the death of the
infracted brain tissue
o Cardiogenic embolic stroke: associated with
cardiac dysrhythmias, usually atrial
fibrillation. Embolic stroke can also be
associated with valvular heart dse and
thrombi in the left ventricle.
o Cryptogenic stoke: which have no cause
o Strokes from other causes: illicit drug use,
coagulopathie, migraine and spontaneous
dissection of the carotid or vertebral artery.
 Pathophysiology
o Disruption of the cerebral blood flow due to
obstruction of a blood vessel → initiates a
complex series of cellular metabolic events
referred to as the ischemic cascade →
Cerebral blood flow decreases to less than
25 mL per 100g per minute → neurons are
no longer maintain aerobic respirations →
mitochondria switch to anaerobic which
generates large amount of lactic acid,
causing a change in the pH level → Neurons
incapable of producing sufficient quantities
of ATP → the membrane pumps electrolyte
balance begin to fail and the cell cease to
function.
o Early in the cascade an area of low cerebral
blood flow, referred to as the penumbra
region, exist around the area of infarction.
The penumbra region is a ischemic brain
tissue that may salvaged with timely
intervention.
o The penumbra area maybe revitalized by
administration of tissue plasminogen
activator.
 Clinical Manifestations
o Numbness or weakness of the face, arm, or
leg, especially on one side of the body
o Confusion or change in mental status
o Trouble speaking or understanding speech
o Visual disturbances
o Difficulty walking, dizziness, or loss of
balance or coordination
o Sudden severe headache

 Motor loss
o A stroke is an upper motor lesion and
results in loss of voluntary control over
motor movements.
o Hemiplegia: paralysis of the face, arm, and
leg on the same side ( due to the lesion on
the opposite hemisphere)
 Nsg Intervention: R.O.M., maintain body
alignment, exercise unaffected limb to
increase mobility, strength and use.
o Hemiparesis: weakness of the face, arm,
and leg on the same side ( due to the lesion
of the opposite side)
 Nsg Intervention: provide object w/in the
pt. reach on the non affected side,
instruct the pt. to increase strength on
unaffected side.
o Ataxia: staggering, unsteady gait; unable to
keep feet together; needs a broad base to
stand
 Sensory Disturbances
 Nsg Intervention: support pt. during the
initial ambulation phase.
 Communication Loss
o Dysarthria: difficulty in forming words
 Nsg intervention: provide pt. w/
alternative method of communication,
allow sufficient to verbal response
o Dysphagia: difficulty in swallowing
 Nsg Intervention: test the pt. pharyngeal
reflexes before offering food or fluid,
place food on the unaffected side of the
mouth.
o Aphasia: loss of speech, could be expressive
aphasia, receptive aphasia, or global
(mixed) aphasia
 Expressive aphasia: unable to form
words that are understandable; may be
able to speak in single word responses
(repeat sounds of the alphabet)
 Receptive aphasia: unable to
comprehend the spoken words; can
speak but may not make sense (speak
slowly and clearly)
 Global (mixed) aphasia: combination of
both receptive and expressive aphasia
(speak clearly and in simple sentences,
use gestures and pictures when able)
o Apraxia: inability to performed previously
learned action
 Visual field deficits
o Homonymous hemianopsia: (loss of the half of
the visual field); unaware of persons or objects
on the side of visual loss, neglect of one side of
the body; difficulty in judging distances.
 Nsg Intervention: place obj w/in intact
field of vision, instruct/ remind pt. to turn
head in the direction of visual loss to
compensate for loss of visual field.
o Loss of peripheral vision: difficulty at seeing at
night, unaware of objects or the borders of
objects
 Nsg Intervention: place obj at the
center intact visual filed, encourage the
use of crane or other objects to identify
objects in the periphery of visual field
o Diplopia: double vision
 Nsg Intervention: explain the location
of object when placing it near the pt.,
consistently place pt. care items in same
location
o Paresthesia: numbness or tingling of the
extremities, difficulty with proprioception
( occurs on the side opposite the lesion)
 Nsg Intervention: ROM, apply
corrective devices as needed
o Agnosias: deficit in the ability to recognize
previously familiar objects perceived by one or
more of the senses.
 Assessment and Diagnostic Findings
o Initial assessment: airway patency (may be
compromised by loss of gag reflexes and
altered respiratory pattern), cardiovascular
status (including BP, cardiac rhythm and rate,
carotid bruit) and gross neurologic deficits.
o A transient ischemic attack (TIA) is a
neurologic deficit lasting less than 24 hours,
w/ most episodes resolving in less than 1 hr.
 Manifested by: sudden loss of motor,
sensory, or visual function. (symp. Results
from temporary ischemia to a specific
region of the brain.) a TIA may serve as a
warning sign of impending stroke.
o Noncontrast CT scan: to determine if the
event is ischemic or hemorrhagic
o 12-lead electrocardiogram (ECG) and carotid
ultrasound are standard test.
 Prevention
o Non-modifiable risk factors
 Advanced age (people older than 55
yrs of age)
 Gender (men have a higher rate of
stroke than women)
 Race (African-American)
o Modifiable risk factors
 Hypertension
 Atrial fibrillation
 Hyperlipidemia
 Obesity
  Smoking
 Diabetes
 Medical Management
o Artrial fibrillation (cardioembolic strokes) are
treated w/ dose-adjusted warfarin sodium
(Coumadin) international normalized ratio: 2.5
(if contraindicated can use aspirin)
o Platelet inhibiting medications; aspirin,
extended-release dipyridamole (Persantine)
plus aspirin, clopidogrel (Plavix), and
ticlopidine (Ticlid); decrease the incidence of
cerebral infarction in pts. who experienced
TIA and stroke from suspected embolic and
thrombotic causes.
o 3-hydroxy-2-methyl-glutaryl-coenzyme A o Skull fracture: is break in the continuity of the
reductase inhibitors (also known as statins)
have been found to reduce coronary events
and strokes; independent of cholesterol levels,
and widely use for stroke prevention.
o Thrombolytic Therapy:
 Dissolving the blood cloth that is
blocking blood flow to the brain.
Recombinant t-Pa is a genetically
engineered form of t-Pa, a thrombolytic
substance made naturally by the body.
Binding to fibrin and converting
plaminogen to plasmin, w/c stimulates
fibrinolysis of the atherosclerotic lesion.
Head Injuries
 Head injury is a broad classification of that
includes injury of the scalp, skull, or brain.
 Pathophysiology
o Brain damage occurs at the moment of impact
o Traumatic injury takes 2 forms:
 Primary Injury: initial damage to the
brain that results from traumatic event.
(Contusions, lacerations and torn blood
vessel due to impact,
acceleration/deceleration, or foreign object
penetration.
 Secondary Injury: evolves over the
ensuing hours and days after the initial
injury and is due primarily due to
unchecked cerebral edema, ischemia and
chemical changes associated with direct
trauma to the brain.
o Bleeding or swelling w/in the skull→ increase the
volume of contents → increases intracranial pressure →
displacement of the brain through or against the rigid
structures of the skull → restriction of blood flow to the
brain→ decreasing oxygen and waste removal→ brain
become anoxic and cannot metabolize properly
producing ischemia, infarction, irreversible brain
damage, and eventually, brain death.
o Brain suffers from traumatic injury → brain swelling or
bleeding; increases intracranial vol. → rigid cranium
allow no room for expansion of contents so intracranial
pressure increases → pressure on blood vessels w/in
the brain causes blood flow to the brain to slow→
cerebral hypoxia and ischemia occur → Intracranial
pressure continues to rise. Brain may herniate. →
cerebral flow ceases
 Scalp Injury: minor injury
o May result in an abrasion (brush wound),
contusions, lacerations or hematoma beneath
the layer of the tissue
o Large-avulsion (tearing away) of the scalp
could be life threatening
o Diagnosis of scalp injury is based on P.E.,
inspection and palpation.
o Area is irrigated b4 the laceration is sutured, to
remove foreign material and to reduce the risk
of infection.
o Subgaleal hematomas (hematoma below the
outer covering of the skull) usually absorb on
their own and do not require any specific
treatment.
 Skull Fracture
skull caused by forceful trauma.
o May occur w/ or w/out damage of the brain
o Classification
 Simple (linear) fracture is a break in
the continuity of the bone.
 A comminuted skull fracture refers to a
splintered or multiple fracture line.
 A fracture of the base of the skull is
called a basilar skull fracture.
o A fracture may be open, indicating a scalp laceration
or tear in the dura or closed, in w/c case the dura is
intact.
Clinical Manifestations
o Persistent localized pain usually suggest that a
fracture is present
o Hemorrhage from the nose, pharynx or ears
and blood may appear under the conjunctiva
o Area a ecchymosis (bruising) may be seen over
the mastoid (battle’s sign)
o Basilar skull fractures are suspected when CSF
escapes from the ear (CSF otorrhea) and nose
(CSF rhinorrhea)
o A halo sign (blood stain surrounded by a
yellowish stain) may be seen in linens or in the
head dressings and is highly suggestive CSF
leak.
Assessment and Diagnostic Findings
o Radiologic Exam confirms the presence and
extent of a skull fracture.
o CT scan: uses high speed x-ray scanning to
detect less apparent abnormalities. Fast,
accurate, and safe diagnostic procedure that
shows the presence, nature, location, and
extent of acute lesion.
o MRI: used to evaluate pts. w/ head injury when
a more accurate picture of the anatomic nature
of the injury is warranted and when the pt. is
stable enough to undergo this longer
procedure.
 Medical Management
o Depressed skull fractures usually require
surgery.
o B4 the surgery: the scalp is shaved and
cleansed with copious amounts of saline to
remove debris.
o Fracture is exposed, skull fragments are
elevated, any underlying dural laceration is
repaired and any accompanying hematoma is
evacuated.
o Penetrating wounds require surgical
debridement to remove foreign bodies and
devitalized brain tissue and to control
hemorrhage
 o IV antibiotic is instituted immediately
o CSF leakage: nasopharynx and external ear
should be kept clean. (Usually piece of sterile
cotton is placed loosely in the ear, or a sterile
cotton pad may be tapped loosely under the
nose or against the ear to collect the draining
fluid.)
o Head is elevated 30 degrees to reduce ICP and
promote spontaneous closure of the leak
Brain Injury
o Brain injury: injury to the brain that is severe enough to
interfere w/ normal functioning.
o Closed (blunt) brain Injury occurs when the head
accelerates and then rapidly decelerates or collides w/
another object (eg. Wall) and brain tissue is damaged
but there is no opening through the skull and dura.
o Open brain injury occurs when an object penetrates
the skull, enters the brain, and damages the soft brain
tissue in its path or when blunt trauma to the head is
so severe that it opens scalp, skull, and dura to expose
the brain.
o Types of Brain Injury
 Concussion: temporary loss of
neurologic function w/ no apparent
structural damage. A concussion also
referred as mild traumatic brain injury
generally involves a period of
unconsciousness lasting from a few
seconds to a few minutes.
* Only cause dizziness and spots in eyes
(“seeing stars”) or it may be severe
enough to cause loss of consciousness for
a time
* If frontal lobe is affected, pt. exhibit
irrational behavior; temporal lobe produce
temporary amnesia or disorientation.
* Treatment involves observing the pt. for
headache, dizziness, lethargy, irritability
and anxiety.
* Postconcussion Syndrome
* Pt family is instructed to observed the ff.
s/sym
-Difficulty in awakening
-Difficulty in speaking
-Confusion
-severe headache
-Vomiting
-weakness of one side of the body
 Contusion: the brain is bruised, w/
possible surface hemorrhage. Pt. is
unconscious for more than few second or
minutes.
* Pt. may lie motionless w/ faint pulse,
shallow respirations, and cool pale skin.
* Often involuntary evacuation of bowels
and bladder occurs.
* May be aroused w/ effort but soon slips
back to unconsciousness.
* BP and Temp are subnormal; similar to
shock
 Diffuse Axonal Injury: involves
widespread damage to axons in the
cerebral hemisphere, corpus callosum and
brain stem. Can be mild, moderate or
severe.
* Pt. experiences no lucid intervals,
immediate coma, decorticate, and
decerebrate posturing.
 Intracranial Hemorrhage: hematoma
maybe epidural (above the dura), subdural
(below the dura) or intracerebral (w/in the
brain). Major symptoms are delayed until
the hematoma is large enough to cause
distortion of the brain and increase ICP.
* Epidural Hematoma (Extradural
Hematoma or Hemorrhage) can result
from a skull fracture that causes a rupture
or laceration of the middle meningeal
artery, the artery that runs between the
dura and the skull inferior to a thin portion
of temporal bone. And usually a
momentary loss of consciousness followed
by interval of apparent recovery (lucid
interval).→ compensation for the
expanding hematoma takes place by rapid
absorption of CSF and decreased
intravascular volume, both of w/c help
maintain normal ICP. But if mechanism no
longer compensates sign of compression
appear (deterioration of consciousness &
signs of focal neurologic deficits, such as
dilation & fixation of pupil or paralysis of
an extremity). Tx: making opening to the
skull (burr holes), ↓ICP, remove cloth &
control bleeding. Craniotomy and drain
may be recquired.
* Subdural hematoma collection of blood
between the dura and the brain, a space
normally occupied by a thin cushion fluid. It
can also occur as a result of coagulopathies
or rupture of an aneurysm. Venous in origin
and is caused by the rupture of small
vessels that bridge the subdural space.
Acute Subdural Hematoma asso. w/ major
injury (contusion & laceration). Clinical
Manifestations develop over 24 to 48 hrs.
S/Sym includes changes in LOC, pupillary
sign and hemiparesis. Subacute Subdural
Hematoma result of less severe contusion
and head trauma. Clinical manifestations
appear 48 hrs. to 2 weeks. Chronic
Subdural Hematoma it is seemly minor
head injury and most common to elderly.
Elderly are prone to this injury secondary
to brain atrophy, w/c is frequent
consequence of the aging process. The
time of the injury and onset of symptoms
can be lengthy. It may be mistaken to
stroke. Bleeding is less profuse but
compression of the intracranial contents
still occurs. The blood w/in the brain
changes in character in 2 to 4 days,
becoming thicker and darker. Cloth breaks
down and has the color and consistency of
motor oil. Symptoms include severe
headache (come & go), alternating focal
neurologic sign, personality changes;
mental deterioration & focal seizures.
* Intracerebral Hemorrhage &
Hematoma is commonly seen in head
injuries when force is exerted to the head
over a small area. Its onset may be
insidious, begin w/ the development of
neurologic deficits ff by headache.
Management includes supportive care,
control of ICP, and careful administration of
fluids and electrolytes and hypertensive
medications.
 Medical Management
 o CT and MRI scans are the primarily control;
independen
neuroimaging diagnostic tools are useful in
t of
evaluating the brain structure. mechanical
o Pt. is transported on a board w/ the head and ventilation
for short
neck maintained in alignment w/ the axis of the periods.
body. C4 Good head Dependent, Dependent Limited to
o A collar spine should be applied until cervical and neck may be voice,
sensation able to eat mouth,
spine x-ray have been obtained and recorded.
and motor w/ adaptive head, chin,
 Brain Death control; sling or shoulder-
o 3 cardinal signs of brain death: coma, absence some controlled
shoulder electric
of brain stem reflexes and apnea.
elevation; wheel chair
o Adjunctive test such as ECG and cerebral blood diaphragm
flow (CBF) studies are often use to confirm movement
C5 Full head Independen Maximal Electric or
brain death.
and neck t w/ assistance modified
control; assistance manual
Spinal Cord Injury shoulder wheel chair,
strength; need
 Pathophysiology
elbow transfer
o Transient concussion (from w/c the pt. full flexion assistance
recovers) to contusion C6 Full Independen Independen Independen
o Laceration and compression of the cord innervated t or w/ t or w/ t in
shoulder, minimal minimal transfers
substance (either alone or combination) wrist assistance assistance and
o Complete transaction (severing) of the cord extension wheelchair
or
(w/c renders the pt. paralyzed below the level
dorsiflexion
of injury) C7 to C8 Fell elbow Independen Independen Independen
o Primary Injuries: Result of the initial assault or extension; t t t, manual
some wheel chair
trauma and usually permanent. finger
o Secondary Injuries: usually the result of a control
T1 to T5 Full hand Independen Independen Independen
contusion or tear injury, in w/c the nerve fibers
finger t t t, manual
begin to swell and disintegrate. control; use wheel chair
o A secondary chain event produces ischemia, of
intercostals
hypoxia, edema and hemorrhagic lesion, w/c in
& thoracic
turn result in destruction of myelin and axons. muscle
 Clinical Manifestations T6 to T10 Abdominal Independen Independen Independen
muscle t t t, manual
o Incomplete Spinal cord lesions (the control, wheel chair
sensory or motor fibers or both are preserved partial to
below the lesion. good
balance w/
o “Neurologic Level” refers to the trunk
lowest level at w/c sensory and motor functions muscles
are normal. Below the neurologic level, there is T11 to L5 Hip flexors, Independen Independen Short
hip t t distance to
total sensory and motor paralysis, loss of abductor full
bladder and bowel control (usually w/ urinary (L1-L3); ambulation
retention and bladder distention), loss of knee w/
extension assistance
sweating and vasomotor tone, and marked (L2-L4),
reduction of BP from loss of peripheral vascular knee
resistance. flexion and
ankle
o Complete Spinal cord lesion: (total
dorsiflexion
loss of sensation and voluntary muscle control (L4-L5)
below the lesion) can result in paraplegia S1 to S5 Full leg, Independen Normal to Ambulate
foot, and t impaired independen
(paralysis of the lower body) or tetraplegia
ankle bowel and tly w/ or
(formerly quadriplegia- paralysis of all 4 control, bladder w/out
extremities). innervation function assistance.
s of
o If conscious the client complains acute
perineal
pain in the back or neck, w/c radiates along the muscles for
involve nerve. bowel,
bladder
and sexual
Injury Segmenta Dressing, Eliminatio Mobility* function
level l eating n
(S2-S4)
Sensorimo
tor
Function  Assessment and Diagnostic Findings
C1 Little of no Dependent Dependent Limited. o Diagnostic X-ray (lateral cervical spine
sensation Voice or
or control sip-n-puff
x-ray) & CT scan
of head controlled o MRI scan: if ligamentous injury is
and neck, electric suspected
no wheel chair
diaphragm  Emergency Management
control; o Pt. must be immobilized on spinal
requires (back) board, w/ head & neck in neural position
continuous
ventilation. o One member of the team must assume
C2 to C3 Head and Dependent Dependent Same as C1 control on the pts. head to prevent flexion,
neck
rotation or extension; done by placing the
sensation;
some neck hands on both sides of the pts. head at about
 ear level to limit movement and maintain
alignment while the spinal board or cervical
immobilizing device is applied.
 Effects of Spinal Cord injuries
o Central Cord Syndrome
 Charac: motor deficit (in the upper
extremities compared to the lower
extremities; sensory loss variesbut is
more pronounced in the upper
extremities), bowel and bladder
dysfunction is variable, or function maybe
completely preserved.
 Cause: injury or edema of the central
cord, usually of the cervical area. May be
caused by hypertension injuries.
o Anterior Cord Syndrome
 Charac: Loss of pain, temp, & motor
function is noted below the level of the
lesion; light touch, position, & vibration
sensation remain intact.
 Cause: The syndrome may be caused by
acute disk hernation of hyperflexion
injuries associated w/ fracture dislocation
of vertebra. Ti may also occur as a result
of injury to the anterior spinal artery, w/c
supplies the anterior two thirds of the
spinal cord.
o Brown-Séquard syndrome (Lateral cord
Syndrome)
 Charac: Ipsilateral paralysis or paresis is
noted, together w/ ipsilateral loss of
touch, pressure, & vibration & measurement are made daily.
contralateral loss of pain and temp.
 Cause: the lesion is caused by a
transverse hemisection of the cord (half of
the cord is transected from north to
south), usually as a result of a knife and
missile injury, fracture-dislocation of
unilateral articular process, or possibly an
acute ruptured disk.
 Medical Management
o Pt. is resuscitated as necessary &
oxygenation & cardiovascular stability are
maintained.
o Pharmacologic Therapy
 High dose corticosteroids, specifically
methylprednisolone found to improve
motor and sensory outcomes
o Respiratory Therapy
 Oxygen is administer to maintained a high
partial pressure of oxygen (Pa02),
because hypoxemia can create or worsen
a neurologic deficit of the spinal cord.
 Diaphragmatic pacing (electrical
stimulation of the pheric nerve) attempts
to stimulate the diaphragm to help pt.
breath.
o Skeletal Fracture Reduction & Traction
 Gardner-Wells tongs require no predrilled
holes in the skull.
 Crutchfield & Vinke tongs are inserted
through holes made in the skull w/ a
special drill under local anesthesia.
 Traction force is exerted along the
longitudinal axis of the vertebral bodies,
w/ the pt. neck in neural position. As the
amount of traction is increased, the
spaces between the intervertebral disks
widen & the vertebrae are given a chance
to slip back into position.
 A halo device may be used initially w/
traction, or may be applied after the
removal of the tongs. It is consisting of a
stainless-steel halo ring that is fixed to the
skull by 4 pins. The pins are attached to a
removable halo vest. It allows
immobilization of the cervical spine while
allowing early ambulation
 Spinal and Neurologic Shock
o Spinal shock asso. w/ SCI reflects a sudden depression
of reflex activity in the spinal cord (areflexia) below the
level of injury. Below level of the lesion are w/out
sensation, paralyzed, & flaccid and reflexes are absent.
Bowel distention & paralytic ileus can be cause by
depression of the reflexes & are treated w/ intestinal
decompression by insertion of nasogastric tube.
o A neurologic shock develops due to the loss autonomic
nervous system function below the level of lesion. The
vital organs are affected, causing BP and heart rate to
↓. This loss of sympathetic innervation → ↓ cardiac
output, venous pooling in the extremities & peripheral
vasodilatation.
 Deep Vein Thrombosis
o Pt. who develop DVT are at risk for pulmonary
embolism (pleuritic chest pain, anxiety, SOB, &
abnormal blood gas values. ↑PaCO2 & ↓
PaO2)
o The pt. should be assessed for a low grade
fever, w/c is 1st sign of DVT, and thigh & calf
o Low dose of anticoagulation therapy usually is
iniated to prevent DVT & PE; thigh-high elastic
compression stockings or pneumatic
compression devices.
 Other Complications
o Respiratory complications
o Autonomic dysreflexia: characterized by
pounding headache, profuse sweating, nasal
congestion, piloerection (“goose bumps”),
bradycardia & hypertension.
Altered Level of Consciousness
 Not oriented, does not follow commands
 Needs persistent stimuli to achieve a state of
alertness
 Loc is gauged on a continuum with a normal state
of alertness and full cognition (consciousness) on
the end and coma on the other.
 Coma is the clinical state of unarousable,
unresponsive in which there is no purposeful
response to internal or external stimuli, although
nonpurposeful responses to painful stimuli & brain
stem reflex may be present
 Akenitic Mutism a state of unresponsiveness to
the environment in which the pt. makes no
voluntary movement
 Persistent Vegetative state a condition in
which the unresponsive pt. resume sleep-awake
cycles after coma but is devoid of cognitive or
affective mental function
 Locked-in-syndrome result from a lesion
affecting the pons, & results in tetraplegia
(quadtriplegia), inability to speak, but vertical eye
movements and lid elevation remain intact and
are used to indicate responsiveness.
 Pathophysiology
o Cause may be neurologic (head injury, stroke)
toxicologic (drug dose, alcohol intoxication) or
metabolic (hepatic or heparin failure, diabetic
ketoacidosis)
o Distruption of the cells of the nervous system,
neurotransmitter or brain anatomy → faulty impulse
transmission → impending communication with the
brain or from the brain to other parts of the body.
These disruptions are caused by cellular edema or
other mechanism
 Clinical Manifestations
o Changes in pupillary responses, eye opening
response, verbal response and motor response
o Initial: subtle behavioral changes such as
restlessness & ↑ anxiety
o Pupils: sluggish, comatose: pupils become
fixed; does not open the eyes
 Assessment and Diagnostic findings
o Evaluation of mental status, cranial nerve
function, cerebellar function (balance &
coordination), reflexes & motor & sensory
function
o Pt. is comatose but pupillary light reflexes are
preserved, a toxic metabolic disorder is
suspected
o Start by assessing the verbal response
o Determining the pt. orientation to time, person
& place assess
o Alertness is measured by the pt. ability to open
eyes spontaneously or response to vocal or
noxious stimulus (pressure or pain)
o Motor response includes spontaneous,
purposeful movement
 Complications
o Respiratory distress/ failure
o Pneumonia
o Aspiration
o Pressure ulcer
o DVT
o Contractures
 Nursing Interventions
o Maintaining airway
 Elevating the head of the bed to 30
degrees helps prevent aspiration
 Positioning the pt. in lateral or semiprone
position also helps, bec it permits the jaw
& tongue to fall forward, thus promoting
drainage of secretions
 Suctioning is performed to remove
secretions from the posterior pharynx and
upper trachea
 Chest physiotherapy & postural drainage
may be initiated to promote pulmonary
hygiene, unless contraindicated by the
pts. underlying condition.
 Chest should be auscultated at least every
8 hours to detect adventitious breath
sounds or absence of breath sounds
o Protecting the Patient
 Side rails are padded
 Providing privacy & speaking to pt. during
nursing activities
o Maintaining Fluid balance and Managing
Nutritional Needs
 IV solutions (blood transfusion) for pt. w/
↑ ICP should be slowly
o Proving Mouth Care
 Mouth is inspected for dryness,
inflammation & crusting
 Unconscious pt. needs continuous oral
care, bec risk of parotitis if the mouth is
not kept scrupulously clean
 Cleansed & rinsed carefully to remove
secretions & crusts & to keep the mucous
membranes moist
 A thin coating of petrolatum on the lips to
prevent drying, cracking & encrustations
 If w/ ET tube; tube should be moved to the
opposite side of the mouth daily to
prevent ulceration of the mouth and lips
o Maintaining skin and joint integrity
 Regular schedule of turning to avoid
pressure
 Turning also provides kinesthetic
(sensation of movement), proprioceptive
(awareness of position) & vestibular
(equilibrium)
 Maintaining correct body position is
important
 Use of splints or foam boots aids in the
prevention of foot drop & use of
torachanter rolls to support the hip joints
keep legs in proper alignment
 Arms are in abduction, finger lightly flexed
and hands in slight supination
o Preserving Corneal Integrity
 Eyes may be cleansed w/ cotton balls
moistened w/ sterile normal saline to
remove debris & discharge
 Cold compress may be prescribed
o Maintaining Body temperature
 Slight elevation of temp may be caused
by dehydration
 Removing all bedding over the pt. (w/ the
possible exception of light sheet or small
drape)
 Administering acetaminophen
 Giving cool sponge bath & allowing
electric fan to blow over the pt. to
increase surface cooling
 Use hypothermia blanket
 Temperature monitoring
o Preventing Urinary Retention
 Bladder is palpated or scanned at
intervals to determine whether urinary
retention is present
 Pt. is not voiding, an indwelling urinary
catheter is inserted & connected to a
close drainage
 A catheter may also be inserted during
the acute phase of illness to monitor
urinary output
 Pt. is observed for fever & cloudy urine
o Promoting Bowel Function
 Abdomen is assessed for distention by
listening for bowel sounds & measuring
the girth of the abdomen w/ tape measure
 Nurse monitors the number & consistency
of bowel movements & performs a rectal
examination for signs of fecal impaction
 Stool softeners may be prescribed
 To facilitate bladder emptying, a glycerin
suppository may be indicated
  Pt. may be require enema every other day
to empty the lower colon
o Providing sensory stimulation
 Nurse touches & talk to the pt. &
encourages family members & friends to
do so. Communication is extremely
important & includes touching the pt. &
spending enough time w/ the pt. to be
become sensitive to his/ her needs
 Nurse orients the pt. to time & place at
least once every 8 hours
 Minimize stimulation by limiting
background noises, having one person to
speak to pt. at a time, giving pt. a longer
time to respond & allowing frequent rest
or quiet times
o Meeting the family needs
o Monitoring & Managing potential complications
 Vital signs & respiratory function are
monitored closely to detect any signs of
respiratory failure or distress
 Chest physiotherapy & suctioning are
initiated to prevent pneumonia
 LOC is monitored closely for evidence of
impaired skin integrity & strategies to
prevent skin breakdown & pressure ulcers
 Care is taken to prevent bacterial
contamination of pressure ulcers, w/c may
lead to sepsis or septic shock
 DVT: prophylaxis such as subcutaneous
heparin or low molecular-wgt heaparin
 Thigh elastic compression sock
Seizures
 Episodes of abnormal motor, sensory, autonomic
or psychic activity (or combination of these) that
result from sudden excessive discharge from
cerebral neurons
 Partial Seizures: begin in one part of the brain
 Partial seizure, consciousness remains intact;
complex partial seizure consciousness is impaired
 Generalized Seizures: involve electrical
discharges in the whole brain
International Classification of Seizures
PARTIAL SIEZURES (SEIZURES BEGINNING
LOCALLY)
Simple Partial Seizures (w/ elementary symptoms,
generally w/out impairment of consciousness)
• w/ motor symptoms
• w/ special sensory or somatosensory symptoms
• w/ autonomic symptoms
• compound forms
Complex Partial seizures (w/ complex symptoms,
generally w/ impairment of consciousness)
• w/ impairment of consciousness only
• w/ cognitive symptoms
• w/ affective symptoms
• w/ psychosensory symptoms
• w/ psychomotor symptoms (automatism)
• Compound forms
Partial seizure secondary generalized
GENERALIZED SEIZURES (CONVULSIVE OR NON
CONVULSIVE, BILATERALLY SYMMETRIC, W/OUT
LOCAL ONSET)
Tonic Clonic seizures
Tonic seizures
Clonic seizures
Absence (petit mal) seizures
Atonic seizures
Myoclonic seizures (bilaterally massive epileptic)
Unclassified seizures
 Cause: Electrical disturbances (dysrhythmia) in
the nerve cell in one section of the brain, these
cells emit abnormal, recurring, uncontrolled
electrical discharges. The characteristic seizure is
a manifestation of excessive neural discharge.
 Asso. Loss of consciousness, excess movement or
loss of muscle tone
 Can be idiopathic (genetic, developmental
defects)
 Acquired seizure:
o Cerebrovascular dse
o Hypoxemia of any cause, including vascular
insufficiency
o Fever (childhood)
o Head injury
o Hypertension
o CNS infection
o Metabolic and toxic conditions (e.g. renal
failure, hyponatremia, hypocalcemia,
hypoglycemia, pesticides)
o Brain tumor
o Drug and alcohol w/drawal
o Allergies
Nursing Management
During Seizure
• The circumstances b4 the seizure
• The occurrence of the aura ( a premonitory or
warning sensation that can be visual, auditory or
olfactory)
• Where the movement or the stiffness begins,
conjugate gaze position and the position of the
head at the beginning of the seizure (gives clues
to the location of the seizure origin in the brain)
• The type of movements in the part of the body
involved
• The areas of the body involved (turn back
bedding to expose pt.)
• The size of both pupils & whether the eyes are
open
• Whether the eyes or the head turn to ones side
• The presence or absence of automatism
(involuntary motor activity, such as lip smacking
or swallowing)
• Incontinence of urine and stool
• Duration of each phase of the seizure
• Unconsciousness
• Any obvious paralysis or weakness of arms or
legs after the seizure
• Inability to speak after the seizure
• Movements at the end of seizure
• Whether or not the patient sleeps afterward
• Cognitive status (confused or not confused)
after the seizure
• PREVENT INJURY
After a Seizure
• The nurse role is to document the events
leading to and occurring during and after the
seizure
• The pt. is at risk for hypoxia, vomiting &
pulmonary aspiration
• To prevent complication: pt. placed in side
lying position to facilitate drainage of oral
secretions & suctioning is performed
 • Bed is placed on a low position w/ two or three
side rails up and padded
Headache
 Head, or cephalgia, is one most common physical
complain
 It may indicate organic dse (neurologic), a stress
response, vasodilation (migraine), skeletal muscle
tension(tension headache)
 Primary headache is one of which no organic
cause can be identified. Types: migraine, tension-
type and cluster headaches.
o Migraine is a symptom complex characterized
by periodic and recurrent attacks of severe
headache lasting from 4 to 72 hrs. in adults. It
is primarily a vascular disturbance that occurs
more commonly in women and has strong
familial tendency
o Tension type headache tend to be chronic
and less severe and are probably the most
common type of headache.
o Cluster headaches are severe form of
vascular headache, frequently in men.
o Cranial arteritis is a cause of headache in the
older population, reaching its incidence in
those older than 70 yrs old. Inflammation of
the cranial arteries is characterized by a severe
headache localized at the region of temporal
arteries.
 Secondary headache: is a symptom associated
w/ an organic cause, such as brain tumor or an
aneurysm.
Assessment and Diagnostic Evaluation
 Detailed history, a PA of head and neck and a
complete neurologic examination
 Headache may be a symptom of endocrine,
hematologic, gastrointestinal, infectious, renal,
cardiovascular or psychiatric dse.
 Medication history: antihypertensive agents,
diuretic medications, anti-inflammatory agents
and monoamine oxidase (MOAI) inhibitor (few
medications that provoke headache)
 Sleep pattern, level of stress, recreational
interests, appetite, recreational interest & family
stressors are relevant
 Questions include:
o Location of headache, does it radiate?
o Quality- dull, aching, steady, boring, burning,
intermittent, continuous, paroxysmal
o Precipitating factors
o What makes head ache worse?
o How long does a typical headache last
o What relieves the headache?
o Does nausea, vomiting, weakness or numbness
in the extremities accompany the headache?
o Insomnia, loss of appetite, loss of energy
o Family history of headache
 Neurologic examination, CT, cerebral
angiography, or MRI may used to detect
underlying causes
 Electromyography (EMG) may reveal a sustained
contraction of the neck, scalp, or facial muscle.
Pathophysiology
 s/symp of migraine result from dysfunction of the
brain stem pathways that normally modulate
sensory input
 Abnormal metabolism of serotonin, a vasoactive
neurotransmitter found in the platelets & cells of
the brain, plays a major role. ( rise in plasma
serotonin, w/c dilates cerebral vessel)
 Migraine can be triggered by : menstrual cycle,
bright lights, stress, depression, sleep deprivation,
fatigue, overuse of certain medications & certain
foods containing tyramine, monosodium
glutamate, nitrites, or milk product & use of oral
contraceptives.
 Emotional or physical stress may cause
contraction of the muscles of the neck & scalp
resulting in tensiousterzn headaches.
 Cluster headache: caused by dilation of orbital
& nearby intracranial arteries
 Cranial arteritis is thought to represent an
immune vasculitis in w/c immune complexes are
deposited w/in the walls of affected blood vessel,
producing vascular injury & inflammation.
Clinical Manifestations
 Migraine: w/ aura can be divided into 4 phases:
• Prodrome: (60%) symptoms occur hrs. to day’s
b4 a migraine headache.
* Symp: depression, irritability, feeling cold,
food cravings, anorexia, change in activity
level, ↑ urination, diarrhea or constipation.
• Aura Phase: (31%); aura usually lasts less than 1 hr &
may provide enough time for pt to take prescribed
medication to avert a full-blown attack.
* Period is characterized by focal neurologic
symptoms, visual disturbances & may be
hemianopic (affecting only half of the visual
field.
* Other symptoms may include numbness &
tingling of the lips, face or hands; mild
confusion; slight weakness of an extremity;
drowsiness & dizziness
* The period of an aura corresponds to the
painless vasoconstriction that is the initial
physiologic change characteristic of classic
migraine
* Cerebral blood flow studies are performed:
during headache demonstrate that during all
phases of the attack, cerebral blood flow is
reduced throughout of the brain, w/
subsequent loss o autoregulation & impaired
carbon dioxide responsiveness.
• Headache Phase: as vasodilation & decline in
serotonin levels occur, a throbbing headache
intensifies over several hours
* This headache is severe & incapacitating & is
often associated w/ photophobia, nausea, &
vomiting. Its duration varies, ranging from 4 to
72 hours.
• Recovery Phase (termination or postdrome):
the pain gradually subsides
*Muscle contraction in the neck & scalp is
common, w/ associated muscle ache &
localized tenderness, exhaustion, & mood
changes
* Any physical exhaustion exaggerates the
headache.
 Tension-type headache: characterized by steady,
constant feeling of pressure that usually begins in
the forehead, temple, or back of the neck.
* Band like or may be described as “a wgt. On top
of my head”
 Cluster headache: unilateral & come in cluster of
one to eight daily, w/ excruciating pain localized
to the eye & orbit & radiating to the facial &
temporal regions.
* The pain is accompanied by watering of the eye
& nasal congestions.
 * Each attack min. to 3 hrs & may have a
crescendo-decrescendo pattern.
* Often described as “penetrating”
 Cranial arteritis: often begins w/ general
manifestations such as fatigue, malaise, wgt loss
& fever.
* Manifestations include inflammation; sometimes
a tender or swollen or nodular temporal artery is
visible.
* Visual problems are caused by ischemia over
involved structure.
Prevention
 Two beta-blocking agents propranolol (Inderal) &
metoprolol (Lopressor) , inhibit the action of beta
receptors- cells in the heart & brain that control
the dilation of blood vessel
Medical Management
 Abortive approach, best employed in those pt.
who have less frequent attacks, is aimed in
relieving or limiting a headache at the onset or
while in progress.
 Preventive approach is used in pt. who experience
more frequent attacks at regular or predictable
intervals & may have a medical condition that
precludes the use of abortive therapies.
 Triptans, serotonin receptor agonist, are the
most specific antimigraine; these agent causes
vasoconstriction, reduce inflammation, & may
reduce pain transmission
• Triptan is Sumatriptan Succinate (Imitrex);
available in oral, intranasal & subcutaneous
preparations & is effective for the treatment of
acute migraine & cluster headaches in adults.
Effective in relieving moderate to severe
migraine headaches in large number of adult
pt. Sumatriptan can cause chest pain & is
contraindicated for pt’s. w/ ischemis heart dse.
• Tiptans should not be taken w/ medications
containing ergotamine, because of potential
prolonged vasoactive reaction.
 Ergotamine tartrate acts on smooth muscle,
causing prolonged constriction of cranial blood
vessels. Side effects include aching muscles,
paresthesias (numbness & tingling), N/V.
 Cafergot, a combination of ergotamine & caffeine,
can arrest or reduce the severity of the headache
if it is taken at the first sign of an attack.
 For acute attack of cluster headache: 100%
oxygen face mask for 15 minutes, ergotamine
tartrate, sumatriptan, corticosteroids or a
percutaneous sphenopalatine ganglion blockade.
 Early administration of a corticosteroid to prevent
the possibility of loss of vision due to vascular
occlusion or rupture of the involved artery.
Nursing Management
 Provide comport measures such as quiet, dark
environment
 Elevation of the head of the bed to 30 degrees
 Symptomatic treatment such as antiemetics may
be indicated
 Symptomatic pain relief for tension headache may
be obtained by application of local heat or
massage.
 Use of analgesic, antidepressant medications &
muscle relaxant.
Meningitis
 Inflammation of the pia mater, the arachnoid &
the CSF- filled subarachnoid space
 Classified into aseptic & septic meningitis.
o Septic meningitis is caused by bacteria
o Aseptic meningitis is caused by viral or
secondary to lymphoma, leukemia or HIV.
Pathophysiology
 Origin: (1) through the blood stream as a
consequence of other infections or (2) by direct
spread, such as might occur after traumatic injury
to the facial bones or secondary to invasive
procedures
 N. meningitis concentrates in the nasopharynx &
is transmitted by secretion or aerosol
contamination.
 Causative organism enters the bloodstream→ it
crosses the blood-brain barrier & proliferates in
the CSF → host immune response stimulates the
release of cell wall fragments &
lipopolysaccharides, facilitating inflammation of
the subarachnoid & pia mater → increased ICP
 CSF circulates through the subarachnoid space,
where inflammatory cellular materials from the
affected meningeal tissue enter & accumulate.
CSF studies demonstrate ↓ glucose, ↑ protein
levels, & ↑ WBC count
Clinical Manifestations
 Headache & fever are frequently the initial
symptoms. Fever tends to remain high throughout
the course; headache is usually either steady or
throbbing & very sever as a result og menigeal
irritation
 Nuchal rigidity (stiff neck): early sign. Any
attempts as flexion of the head are difficult
because of spasms in the muscle of the neck.
Forceful flexion causes severe pain.
 (+) Kernig’s sign: when the pt. is lying w/ the
thigh flexed on the abdomen, the leg cannot be
completely extended
 (+) Brudzinski’s sign: when the pt. neck is flexed
(after ruling out cervical trauma or injury), flexion
of the knees & hips is produced; when the lower
extremity of one side is passively flexed, a similar
movement is seen in the opposite extremity. More
sensitive indication of meningeal irritation.
 Photophobia(extreme sensitivity to light)
 Rash can be striking feature of N. meningitis
infection
 Skin lesions develop, ranging from a petechial
rash w/ purpuric lesions to large areas of
ecchymosis
 Disorientation & memory impairment
 Behavioral manifestations; as illness progress,
lethargy, unresponsiveness & coma may develop.
 Seizures in adults w/ S.pneumoniae meningitis &
are the result of areas irritability in the brain → ICP
↑ secondary to the accumulation of purulent
exudates (initial signs of ↑ ICP include: ↓ LOC &
fucal motor deficits). If ICP is not controlled, the
uncus of the temporal lobe may herniate through
the tentorium, causing pressure on the brain
stem.
 Acute fulminant infection producing signs of
overwhelming septicemia: an abrupt onset of high
fever, extensive purpuric lesions (over the face &
extremities), shock & signs of disseminated
intravascular coagulopathy.
Assessment and Diagnostic Findings
 Bacterial culture & Gram staining of CSF & blood
are key diagnostic test.
 Presence of polysaccharide antigen in CSF further
supports the diagnosis of bacterial meningitis.
Medical Management
 Penicillin antibiotic (eg. Ampicillin, pipercillin)
 Cephalosporins
 Vancomycin hydrochloride alone or in
combination w/ rifampin may be used if resistant
strains of bacteria are identified.
 Dexamethasone has been shown to be beneficial
as adjunct therapy in the treatment of acute
bacterial meningitis & in pneumococcal meningitis
if it is administered 15 to 20 minutes b4 the 1st
dose of antibiotic & every 6 hours for the next 4
days.
Nursing Management
 Neurologic status & vital signs are continually
assessed
 Pulse oximetry & arterial blood gas values are
used to quickly indentify the need for respiratory
support in ↑ ICP compromises the brain stem
 Insertion of a cuffed endotracheal tube &
mechanical ventilation may be necessary to
maintain adequate tissue oxygenation.
 Arterial blood pressure are monitored to assess
incipient shock
 Measures are taken to reduce body temperature
as quickly as possible. (Fever also increases the
workload of the heart & cerebral metabolism. ICP
will increase in response to the increased cerebral
metabolic demands)
 Protecting the pt. form injury secondary to seizure
activity or altered LOC
 Monitoring body wgt daily
 Preventing complications associated w/ immobility
such as pressure ulcers & pneumonia
BRAIN ABSCESS
Pathophysiology
 Brain abscess is a collection of infectious material
w/in the tissue of the brain
 Most common predisposing conditions for abscess
among immunocompetent adults w/ otitis media &
sinusitis
 An abscess can result form intracranial surgery,
penetrating head injury, or tongue piercing
 Organism causing brain abscess may reach the
brain by hematologic spread from the lungs,
gums, tongue or heart or from a wound or intra-
abdominal infection
 To prevent brain abscess, otitis media,
mastoiditis, sinusitis, dental infections & systemic
infections should be treated promptly.
Clinical Manifestations
 Manifestations result form alterations in
intracranial dynamics (edema, brain shift),
infection, or the location of the abscess.
 Headache, usually worse in the morning, is the
most prevailing symptoms.
 Fever, vomiting, & focal neurologic deficits occurs
as well.
 Focal deficits such as weakness & decreasing
vision reflect the area of brain that is involved.
 As abscess expands symp. Of increase ICP such as
decreasing LOC & seizures are observed.
Assessment and Diagnostic Findings
 Neurologic studies such as MRI and CT identify the
size & location of the abscess.
 Aspiration of the abscess, guided by CT or MRI is
the best method to culture & identify the
infectious organism.
Medical Management
 Treatment is aimed at controlling the increased
ICP, draining the abscess & providing
antimicrobial therapy directed at the abscess &
the primary source of infection.
 Corticosteroids may be prescribed to help reduce
the inflammatory cerebral edema if the pt shows
evidence of an increasing neurologic deficit.
Nursing Management
 Continuing to assess the neurologic status,
administering medications, assessing the
response to treatment and providing supportive
care.
 Ongoing neurologic assessment alerts the nurse
to changes in ICP
 The nurse also assesses and documents the
responses to medications
 Administration of insulin or electrolyte
replacement may be required to return these
values to normal or acceptable levels.
 Pt. safety is another key nursing responsibility.
MULTIPLE SCLEROSIS
 Multiple sclerosis (MS) is an immune-mediated,
progressive demyelinating dse of the CNS.
 Demyelination refers to the destruction of myelin,
the fatty & protein material that surrounds certain
nerve fibers in the brain & spinal cord; it result in
impaired transmission of nerve impulses.
 Genetic predisposition is indicated by the
presence of a specific cluster (haplotype) of
human leukocyte antigens (HLA) on the cell wall.
Presence of this haplotype may promote
susceptibility to factors, such as viruses, that
trigger the autoimmune response activated in MS.
 DNA on the viruses mimics the amino acid
sequence of myelin, resulting in an immune
system cross-section in the presence of a
defective immune system.
Pathophysiology
 Sensitized T cells typically cross the blood-brain
barrier: their function is to check the CNS for
antigens & then leave.
 Sensitized T cells remain in the CNS & promote
filtration of other agents that damage the immune
system → immune system attack leads to
inflammation that destroys myelin (w/c normally
insulates the axon & speeds the conduction of
impulses along the axon.) → the oligodendroglial
cells that produce myelin in the CNS.
 Demyelination interrupts the flow of nerve
impulses & results in variety of manifestations.
 Plaques appear on demyelinated axons, further
interrupting the transmission of impulses.
Demyelinated axons are scattered irregularly
throughout the CNS.
 Areas most frequently affected are the optic
nerves, chiasm, and tracts; the cerebrum; the
brain stem & cerebellum; and spinal cord.
 Eventually, the axons themselves begin to
degenerate, resulting in permanent & irreversible
damage.
Clinical Manifestations
 Benign course & symptoms are so mild that the
pt. does not seek health care or treatment
 Primary progressive MS may result in
quadriparesis, cognitive dysfunction, visual loss &
brain stem syndromes.
 Primary symptoms: fatigue, depression,
weakness, numbness, difficulty in coordination,
loss of balance, & pain.
 Visual disturbances due to lesions in the optic
nerves or their connections may include blurring
 of vision, diplopia (double vision), patchy
blindness (scotoma) and total blindness.
 Fatigue is defined as a subjective lack of physical
or mental energy that interferes w/ desired
activity.
 Depression, heat, anemia, deconditioning &
medication may contribute to fatigue.
 Avoiding heat temperatures, effective treatment
of depression & anemia, and physical therapy my
control fatigue.
 Lesions on the sensory pathways cause pain.
 Additional sensory manifestations: paresthesias,
dysesthesias & propprioception loss.
 Spasticity (muscle hypertonicity) of
extremities and loss of the abdominal reflexes
result from involvement of the main motor
pathways (pyramidal tracts) of the spinal cord.
 Disruption of the sensory axons may produce
sensory dysfunction (paresthesias, pain).
 Cognitive & psychosocial problems may reflect
frontal or parietal lobe involvement.
 Involvement of the cerebellum or basal ganglia
can produce ataxia (impaired coordination of
movements) and tremor.
 Loss of control connections between the cortex
and the basal ganglia may occur and cause
emotional lability and euphoria.
 Bladder, bowel and sexual dysfunctions are
common.
 Secondary complications: UTI, constipation,
pressure ulcers, contracture deformities,
dependent pedal edema, pneumonia, reactive
depression & decreased bone density.
 Exacerbations & remissions are characteristics of
MS.
o Exacerbations: new symptoms appear and
existing ones worsen
o Remission: symptoms decrease or disappear.
Glossary
 Agnosias: loss of ability to recognize objects
through a particular sensory system; may be
visual, auditory or tactile.
 Akathesia: restlessness, urgent need to move
around, and agitation
 Akinetic Mutism: unresponsiveness to the
environment; the patient makes no movement or
sound but sometimes opens the eye
 Altered level of consciousness: condition of
being less responsive to & aware of environmental
stimuli
 Aneurysm: a weakening or bulge in an arterial
wall
 Aphasia: inability to express oneself or to
understand language
 Apraxia: inability to performed previously
learned purposeful motor acts on a voluntary
basis
 Ataxia: impaired ability to coordinate movement,
often seen as a staggering gait or postural
imbalance
 Autonomic dysreflexia: a life threatening
emergency in spinal cord injury pr that causes a
hypertensive emergency; also called autonomic
hyperreflexia
the
 Autoregulation: ability of cerebral blood vessels
to dilate or constrict to maintain stable cerebral
blood flow despite changes in systemic arterial BP
 Autonomic nervous system: division of nervous
system that regulates the involuntary body
functions.
 Axon: portion of neuron that conducts impulses
away from the cell body.
 Babiski reflex (sign): a reflex action of the toes;
indicative of abnormalities in the motor control
pathways leading form the cerebral cortex.
 Bradykinesia: very slow voluntary movements
and speech
 Brain injury: an injury to the skull or brain that is
severe enough to interfere w/ normal functioning
 Brain injury, closed(blunt): occurs when head
accelerates and then rapidly decelerates or
collides w/ another object and the brain tissue
damage, but there is no opening through the skull
and dura
 Brain injury, open: occurs when an object
penetrates the skull, enters the brain and
damages the soft brain tissue in its path
(penetrating injury), or when blunt trauma to the
head is so severe that it opens the scalp, skull,
and dura to expose the brain
 Brain death: irreversible loss of all functions of
the entire brain, including brain stem
 Bulbar paralysis: immobility of muscles
innervated by cranial nerves w/ their cell bodies in
the lower portion of the brain stem
 Chorea: rapid, jerky, involuntary, purposeless
movement of the extremities or facial muscles,
including facial grimace
 Clonus: abnormal movement marked by
alternating contraction and relaxation of a muscle
occurring in rapid succession.
 Coma: prolonged state of unconsciousness
 Complete spinal cord lesion: a condition
involves total loss of sensation and voluntary
muscle control below the lesion
 Concussion: a temporary loss of neurologic
function w no apparent structural damage to the
brain
 Contusion: bruising damage to the brain surface
 Craniectomy: a surgical procedure that involves
removal of a portion of the skull
 Cushing response: brains attempts to restore
blood flow by increasing arterial pressure to
overcome the increased intracranial pressure
 Decerebration: an abnormal body posture asso
w/ a severe brain injury, characterized by extreme
extension of the upper and lower extremities
 Decortications: an abnormal posture asso w/ a
severe brain injury, characterized by extreme
flexion of the upper and lower extremities
 Delirium: transient loss of intellectual function,
usually due to systemic problems
 Dementia: a progressive organic mental disorder
characterized by personality changes, confusion,
disorientation, and deterioration of intellect asso
w/ impaired memory and judgement
 Dendrite: portion of the neuron that conducts
impulses toward the cell body.
 Diplopia: double vision, or the awareness of two
images of the same objectoccuring in one or both
eyes
 Dsyphagia: difficulty in swallowing, causing the
pt to at risk for aspiration
 Dysphonia: voice impairment or altered voice
production and incoordination of muscles
responsible to speech
 Dysarthria: defects of articulation due to
neurologic causes
 Dyskinesias: impaired ability to execute
voluntary movements
 Epidural monitor: a sensor placed between the
skull & the dura to monitor intracranial pressure
 Epilepsy: a group of syndromes characterized by
paroxysmal transient disturbances of brain
function
 Expressive aphasia: inability to express oneself
due; often asso w/ damage to the left frontal lobe
 Fiberoptic monitor: a system that uses light
refraction to determine intracranial pressure
 Flaccid: displaying lack of muscle tone, limp,
floppy
 Halo-vest: a lightweight vest w/ an attached halo
that stabilizes the cervical spine
 Head injury: an injury to the scalp, skull, and/or
brain
 Hemianopsia: blindness of half, of the field of
vision in one or both eyes
 Hemeplegia/hemiparesis: weakness/ paralysis
of one side of the body, or part of it, due to an
injury to the motor areas of the brain
 Hernation: abnormal protrusion of tissue through
a defect or natural opening
 Incomplete spinal cord lesion: a condition
where there is preservation of the sensory or
motor fibers, or both, below the lesion
 Infarction: a zone of tissue deprived of blood
supply
 Intracranial pressure: pressure exerted by the
vol. of the intracranial contents w/in the cranial
vault
 Korsakoff’s syndrome: personality disorder
characterized by psychosis, disorientation,
delirium, insomnia & hallucination
 Locked-in syndrome: condition resulting from a
lesion in the pons in w/c the pt lacks all distal
motor activity (tetraplegia) but cognition is intact.
 Microdialysis: procedure in w/c an intracranial
catheter is inserted near an injured area of the
brain to measure lactate, pyruvate, glutamate and
glucose levels
 Micrographia: small and often illegible
handwrtting
 Migraine headache: a severe, unrelenting
headache often accompanied by symptoms such
as nausea, vomiting and visual disturbances
 Monro-Kellie hypothesis: because of limited
space in the skull, an increase in any one skull
component—brain tissue, blood, or CSF—will
cause a change in the volume of the others
 Neurologic bladder: bladder dysfunction that
results from a disorder or dysfunction of the
nervous system; may lead result in either urinary
retention or bladder overactivity
 Neurodegenerative: a dse, or condtion that
leads to deterioration of normal clees or function
of the nervous system
 Neuropathy: general term indicating a disorder
of the nervous system
 Papilledema: edema of the optic nerve
 Paraplegia: paralysis of the lower extremities w/
dysfunction of the bowel and bladder from a
lesion in the thoracic, lumbar, or sacral regions of
the spinal cord
 Parasympathetic nervous system: division of
the ANS active primarily during nonstressful
conditions, controlling mostly visceral functions.
 Paresthesias: a sensation numbness or tingling
or a “pins” and “needles” sensation
 Penumbra region: area of flow cerebral blood
flow
 Persistent vegetative state: condition in w/c
the pt is wakeful but devoid of conscious content,
w/out cognitive or affective mental function
 Photophobia: inability to tolerate light
 Position (postural) sense: awareness of
position of parts of the body w/out looking at
them, also referred to as proprioception
 Primary headache: a headache for w/c no
specific organic cause can be found
 Prion: a particle smaller than a virus that is
resistant to standard sterilization procedures
 Radioculopathy: dse of spinal nerve root, often
resulting in pain and extreme sensitivity to touch
 Reflex: an automatic response stimuli
 Receptive aphasia: inability to understand what
someone else is saying; often asso w/ damage to
the temporal area
 Rigidity: increase in muscle tone at rest
characterized by increased resistance to passive
stretch.
 Romberg test: test for cerebellar dysfunction
requiring the pt to stand w/ feet together, eyes
closed and arms extended; inability to maintain
the position, w/ either significant stagger or sway,
is a (+) test.
 Sciatica: inflammation of sciatic nerve, resulting
in pain and tenderness along the nerve through
the thigh and leg
 Secondary headache: headache identified as a
symptom of another organic disorder
 Secondary injury: an insult to the brain
subsequent to the original traumatic event
 Seizures: paroxysmal transient disturbance of
the brain resulting from a discharge of abnormal
electrical activity
 Spasticity: sustained increase tension of a
muscle when it is passively lengthened or
stretched; hypertonicity w/ increased resistance to
 stretch often asso w/ weakness, increased deep
tendon reflexes and diminished superficial
reflexes
 Spinal cord injury: an injury to the spinal cord,
vertebral column, supporting soft tissue or
intervertebral disk caused by trauma
 Spondylosis: ankylosis or stiffening if the
cervical or lumbar vertebrae
 Spongiform: having the appearance or quality of
a sponge
 Status epilepticus: episode in w/c the pt.
experiences multiple seizure bursts w/ no
recovery time between
 Sunarachnoid screw or bolt: device placed into
the subarachnoid space to measure intracranial
pressure
 Sympathetic Nervous System: division of the
ANS w/ predominantly excitatory responses, the
“fight-or-flight” system
 Tetraplegia (quadriplegia): paralysis of both
arms and legs, w/ dysfunction of bowel and
bladder from a lesion of the cervical segments of
the spinal cord
 Tone: tension present in a muscle at rest
 Transaction: severing of the spinal cord itself;
transaction can be complete (all the way through
the cord) or incomplete (partially through)
 Transsphenoidal: surgical approach to the
pituitary via the sphenoid sinuses
 Ventriculostomy: a catheter placed in one
lateral ventricles of the brain to measure
intracranial pressure and allow for drainage of
fluid
 Vertigo: an illusion of movement, usually rotation