Neurological Dysfuntion
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KOMUNITAS BLOGGER UNIVERSITAS SRIWIJAYA
Increased (ICP) Intracranial Pressure Ø Intracranial pressure more than 15 mmHg
Ø Brunner= Normal intracranial pressure 10-20 mmHg Ø 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 Ø Compensation to maintain a normal ICP of 10 to 20 mm Hg is normally
accomplished by shifting or displacing CSF Ø With disease or injury, ICP may
increase Ø Increased ICP decreases cerebral perfusion, causes ischemia, cell death,
and (further) edema Ø Brain tissues may shift through the dura and result in
herniation Ø Autoregulation: refers to the brain’s ability to change the diameter
of blood vessels to maintain cerebral blood flow during alterations in the systemic blood
pressure Ø CO2 plays a role; decreased CO2 results in vasoconstriction, and
increased CO2 results in vasodilatation Ø Pathophysiology · The cranium
only contains the brain substance, the CSF and the blood/blood vessels · MONROKELLIE 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
Ø 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 o Increased concentration of carbon dioxide
will cause VASODILATION à increased flowà increased ICP Ø
Cerebral Edema o Abnormal accumulation of fluid in the intracellular space, extracellular
space or both. o Edema can occur in gray, white or interstitial matter. Ø Herniation
· Results from an excessive increase in ICP when the pressure builds up and the
brain tissue presses down on the brain stem Ø Cerebral response to increased ICP
· The brain can maintain a steady perfusion pressure if the arterial systolic blood
pressure is 50 to 150 mm Hg and the ICP is less than 40 mm Hg · 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 ü
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
movements(Pupillary changes- fixed, slowed response) o Weakness in one extremity or one
side o Headache: constant, increasing in intensity, or aggravated by movement or straining o
Vomiting o Comatose and abnormal motor response in the form of decortication (abnormal
flexion of the upper extremities and extension of the lower extremities), decerbration
(extreme extension of the upper and lower extremities) of flaccidity ü Manifestations of
Increased ICP—Late o Respiratory and vasomotor changes o VS: increase in systolic
blood pressure, widening of pulse pressure, and slowing of the heart rate; pulse may
fluctuate rapidly from tachycardia to bradycardia and temperature increase §
Cushing’s triad: bradycardia, hypertension, and bradypnea o Projectile vomiting o
Hyperthermia o Abnormal posturing ü Complications o Brain stem herniation: results
from an excessive increase in ICP in which the pressure builds in the cranial vault and the
brain tissue presses down on the brain stem. Results in cessation of blood flow to the brain,
leading to irreversible brain anoxia and brain death. o Diabetes Insipidus: results of
decreased secretion of ADH s/symp: excessive urine output, decreased urine osmolality and
serum hyperosmolality o SIADH: is the result of increased secretion of ADH. Pt. becomes
vol. overloaded, urine output diminishes, and serum sodium concentration becomes dilute. o
Nursing Process—Assessment of the Patient With Increased Intracranial Pressure o
Conduct frequent and ongoing neurologic assessment o Evaluate neurologic status as
completely as possible o Glasgow Coma Scale o Pupil checks o Assess selected cranial
nerves o Take frequent vital signs o Assess intracranial pressure o Nursing interventions: o
Maintain patent airway § 1. Elevate the head of the bed 15-30 degrees- to promote
venous drainage § 2. assists in administering 100% oxygen or controlled
hyperventilation- to reduce the CO2 blood levelsàconstricts blood
vesselsàreduces edema § 3. Administer prescribed medications- usually
· Mannitol- to produce negative fluid balance · corticosteroid- to reduce
edema · anticonvulsants-p to prevent seizures § 4. Reduce environmental
stimuli § 5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and
vigorous suctioning § 6. Keep head on a neutral position. ACOID- extreme flexion,
valsalva § 7. monitor for secondary complications · Diabetes insipidus- output of
>200 mL/hr · SIADH ü Medical Management: o Monitoring Intracranial
Pressure and Cerebral Oxygenation: § Ventriculostomy: a fine-bore catheter is inserted
into a lateral ventricle, preferably in the non dominant hemisphere of the brain. Use to drain
blood from the ventricle. Continuous drainage of CSF under pressure control is an effective
method 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 transducertipped 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 Ø Sudden
loss of function resulting from disruption of the blood supply to a part of the brain. Ø
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. Ø 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. Ø 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 Ø 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 § Nsg
Intervention: support pt. during the initial ambulation phase. Ø 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 Ø 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 Ø Sensory Disturbances 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.
ü 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. ü 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 ü 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 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 Ø Head injury is a broad
classification of that includes injury of the scalp, skull, or brain. Ø 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 v 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. v Skull Fracture o Skull
fracture: is break in the continuity of the 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. ü 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. ü 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. ü 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 v 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. ü Medical Management o CT and MRI scans are the primarily
neuroimaging diagnostic tools are useful in evaluating the brain structure. o Pt. is transported
on a board w/ the head and neck maintained in alignment w/ the axis of the body. o A collar
spine should be applied until cervical spine x-ray have been obtained and recorded. ü
Brain Death o 3 cardinal signs of brain death: coma, absence of brain stem reflexes and
apnea. o Adjunctive test such as ECG and cerebral blood flow (CBF) studies are often use to
confirm brain death. Spinal Cord Injury Ø Pathophysiology o Transient concussion
(from w/c the pt. full recovers) to contusion o Laceration and compression of the cord
substance (either alone or combination) o Complete transaction (severing) of the cord (w/c
renders the pt. paralyzed below the level of injury) o Primary Injuries: Result of the initial
assault or trauma and usually permanent. o Secondary Injuries: usually the result of a
contusion or tear injury, in w/c the nerve fibers begin to swell and disintegrate. o A secondary
chain event produces ischemia, hypoxia, edema and hemorrhagic lesion, w/c in turn result in
destruction of myelin and axons. Ø Clinical Manifestations o Incomplete Spinal cord
lesions (the sensory or motor fibers or both are preserved below the lesion. o
“Neurologic Level” refers to the lowest level at w/c sensory and motor functions
are normal. Below the neurologic level, there is total sensory and motor paralysis, loss of
bladder and bowel control (usually w/ urinary retention and bladder distention), loss of
sweating and vasomotor tone, and marked reduction of BP from loss of peripheral vascular
resistance. o Complete Spinal cord lesion: (total loss of sensation and voluntary muscle
control below the lesion) can result in paraplegia (paralysis of the lower body) or tetraplegia
(formerly quadriplegia- paralysis of all 4 extremities). o If conscious the client complains
acute pain in the back or neck, w/c radiates along the involve nerve. Injury level Segmental
Sensorimotor Function Dressing, eating Elimination Mobility* C1 Little of no sensation or
control of head and neck, no diaphragm control; requires continuous ventilation. Dependent
Dependent Limited. Voice or sip-n-puff controlled electric wheel chair C2 to C3 Head and
neck sensation; some neck control; independent of mechanical ventilation for short periods.
Dependent Dependent Same as C1 C4 Good head and neck sensation and motor control;
some shoulder elevation; diaphragm movement Dependent, may be able to eat w/ adaptive
sling Dependent Limited to voice, mouth, head, chin, or shoulder-controlled electric wheel
chair C5 Full head and neck control; shoulder strength; elbow flexion Independent w/
assistance Maximal assistance Electric or modified manual wheel chair, need transfer
assistance C6 Full innervated shoulder, wrist extension or dorsiflexion Independent or w/
minimal assistance Independent or w/ minimal assistance Independent in transfers and
wheelchair C7 to C8 Fell elbow extension; some finger control Independent Independent
Independent, manual wheel chair T1 to T5 Full hand finger control; use of intercostals &
thoracic muscle Independent Independent Independent, manual wheel chair T6 to T10
Abdominal muscle control, partial to good balance w/ trunk muscles Independent
Independent Independent, manual wheel chair T11 to L5 Hip flexors, hip abductor (L1-L3);
knee extension (L2-L4), knee flexion and ankle dorsiflexion (L4-L5) Independent
Independent Short distance to full ambulation w/ assistance S1 to S5 Full leg, foot, and ankle
control, innervations of perineal muscles for bowel, bladder and sexual function (S2-S4)
Independent Normal to impaired bowel and bladder function Ambulate independently w/ or
w/out assistance. Ø Assessment and Diagnostic Findings o Diagnostic X-ray (lateral
cervical spine x-ray) & CT scan o MRI scan: if ligamentous injury is suspected Ø
Emergency Management o Pt. must be immobilized on spinal (back) board, w/ head &
neck in neural position o One member of the team must assume control on the pts. head to
prevent flexion, rotation or extension; done by placing the 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. Ø 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 BrownSéquard syndrome (Lateral cord Syndrome) § Charac: Ipsilateral paralysis or
paresis is noted, together w/ ipsilateral loss of touch, pressure, & vibration &
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. Ø 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 Ø 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.
Ø 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 measurement are made daily. o Low dose of anticoagulation therapy usually
is iniated to prevent DVT & PE; thigh-high elastic compression stockings or pneumatic
compression devices. Ø 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 Ø Not oriented, does not follow commands Ø
Needs persistent stimuli to achieve a state of alertness Ø Loc is gauged on a
continuum with a normal state of alertness and full cognition (consciousness) on the end and
coma on the other. Ø 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 Ø Akenitic
Mutism a state of unresponsiveness to the environment in which the pt. makes no voluntary
movement Ø 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
Ø 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. Ø 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 Ø 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 Ø
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 Ø Complications o
Respiratory distress/ failure o Pneumonia o Aspiration o Pressure ulcer o DVT o
Contractures Ø 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 Ø Episodes of abnormal motor, sensory,
autonomic or psychic activity (or combination of these) that result from sudden excessive
discharge from cerebral neurons Ø Partial Seizures: begin in one part of the brain
Ø Partial seizure, consciousness remains intact; complex partial seizure
consciousness is impaired Ø 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 Ø 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. Ø Asso. Loss of consciousness, excess movement or loss of muscle tone
Ø Can be idiopathic (genetic, developmental defects) Ø 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 Ø Head, or cephalgia, is one most
common physical complain Ø It may indicate organic dse (neurologic), a stress
response, vasodilation (migraine), skeletal muscle tension(tension headache) Ø
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.
Ø Secondary headache: is a symptom associated w/ an organic cause, such as brain
tumor or an aneurysm. Assessment and Diagnostic Evaluation Ø Detailed history, a
PA of head and neck and a complete neurologic examination Ø Headache may be a
symptom of endocrine, hematologic, gastrointestinal, infectious, renal, cardiovascular or
psychiatric dse. Ø Medication history: antihypertensive agents, diuretic medications,
anti-inflammatory agents and monoamine oxidase (MOAI) inhibitor (few medications that
provoke headache) Ø Sleep pattern, level of stress, recreational interests, appetite,
recreational interest & family stressors are relevant Ø 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 Ø Neurologic
examination, CT, cerebral angiography, or MRI may used to detect underlying causes
Ø Electromyography (EMG) may reveal a sustained contraction of the neck, scalp, or
facial muscle. Pathophysiology Ø s/symp of migraine result from dysfunction of the
brain stem pathways that normally modulate sensory input Ø 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) Ø 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. Ø Emotional or
physical stress may cause contraction of the muscles of the neck & scalp resulting in
tensiousterzn headaches. Ø Cluster headache: caused by dilation of orbital &
nearby intracranial arteries Ø 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 Ø 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.
Ø 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” Ø 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” Ø
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 Ø 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 Ø 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. Ø 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. Ø 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. Ø Ergotamine tartrate acts on smooth
muscle, causing prolonged constriction of cranial blood vessels. Side effects include aching
muscles, paresthesias (numbness & tingling), N/V. Ø 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. Ø For acute attack of cluster headache: 100% oxygen face
mask for 15 minutes, ergotamine tartrate, sumatriptan, corticosteroids or a percutaneous
sphenopalatine ganglion blockade. Ø 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 Ø Provide comport measures such as quiet, dark
environment Ø Elevation of the head of the bed to 30 degrees Ø Symptomatic
treatment such as antiemetics may be indicated Ø Symptomatic pain relief for tension
headache may be obtained by application of local heat or massage. Ø Use of
analgesic, antidepressant medications & muscle relaxant. Meningitis Ø
Inflammation of the pia mater, the arachnoid & the CSF- filled subarachnoid space
Ø 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 Ø 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 Ø N. meningitis concentrates in the
nasopharynx & is transmitted by secretion or aerosol contamination. Ø
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 Ø 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 Ø 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 Ø 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. Ø (+)
Kernig’s sign: when the pt. is lying w/ the thigh flexed on the abdomen, the leg cannot
be completely extended Ø (+) 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. Ø
Photophobia(extreme sensitivity to light) Ø Rash can be striking feature of N.
meningitis infection Ø Skin lesions develop, ranging from a petechial rash w/ purpuric
lesions to large areas of ecchymosis Ø Disorientation & memory impairment
Ø Behavioral manifestations; as illness progress, lethargy, unresponsiveness &
coma may develop. Ø 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. Ø 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 Ø Bacterial culture & Gram staining of
CSF & blood are key diagnostic test. Ø Presence of polysaccharide antigen in
CSF further supports the diagnosis of bacterial meningitis. Medical Management Ø
Penicillin antibiotic (eg. Ampicillin, pipercillin) Ø Cephalosporins Ø
Vancomycin hydrochloride alone or in combination w/ rifampin may be used if resistant
strains of bacteria are identified. Ø 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 Ø Neurologic status & vital
signs are continually assessed Ø Pulse oximetry & arterial blood gas values are
used to quickly indentify the need for respiratory support in ↑ ICP compromises the
brain stem Ø Insertion of a cuffed endotracheal tube & mechanical ventilation
may be necessary to maintain adequate tissue oxygenation. Ø Arterial blood
pressure are monitored to assess incipient shock Ø 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) Ø Protecting the pt. form injury secondary to seizure activity or
altered LOC Ø Monitoring body wgt daily Ø Preventing complications
associated w/ immobility such as pressure ulcers & pneumonia BRAIN ABSCESS
Pathophysiology Ø Brain abscess is a collection of infectious material w/in the tissue
of the brain Ø Most common predisposing conditions for abscess among
immunocompetent adults w/ otitis media & sinusitis Ø An abscess can result
form intracranial surgery, penetrating head injury, or tongue piercing Ø 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 Ø To prevent brain
abscess, otitis media, mastoiditis, sinusitis, dental infections & systemic infections
should be treated promptly. Clinical Manifestations Ø Manifestations result form
alterations in intracranial dynamics (edema, brain shift), infection, or the location of the
abscess. Ø Headache, usually worse in the morning, is the most prevailing
symptoms. Ø Fever, vomiting, & focal neurologic deficits occurs as well.
Ø Focal deficits such as weakness & decreasing vision reflect the area of brain
that is involved. Ø As abscess expands symp. Of increase ICP such as decreasing
LOC & seizures are observed. Assessment and Diagnostic Findings Ø
Neurologic studies such as MRI and CT identify the size & location of the abscess.
Ø Aspiration of the abscess, guided by CT or MRI is the best method to culture
& identify the infectious organism. Medical Management Ø Treatment is aimed
at controlling the increased ICP, draining the abscess & providing antimicrobial therapy
directed at the abscess & the primary source of infection. Ø Corticosteroids may
be prescribed to help reduce the inflammatory cerebral edema if the pt shows evidence of an
increasing neurologic deficit. Nursing Management Ø Continuing to assess the
neurologic status, administering medications, assessing the response to treatment and
providing supportive care. Ø Ongoing neurologic assessment alerts the nurse to
changes in ICP Ø The nurse also assesses and documents the responses to
medications Ø Administration of insulin or electrolyte replacement may be required to
return these values to normal or acceptable levels. Ø Pt. safety is another key nursing
responsibility. MULTIPLE SCLEROSIS Ø Multiple sclerosis (MS) is an immunemediated, progressive demyelinating dse of the CNS. Ø 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. Ø
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. Ø 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 Ø Sensitized T cells typically cross the blood-brain barrier: their
function is to check the CNS for antigens & then leave. Ø 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. Ø Demyelination interrupts the
flow of nerve impulses & results in variety of manifestations. Ø Plaques appear
on demyelinated axons, further interrupting the transmission of impulses. Demyelinated
axons are scattered irregularly throughout the CNS. Ø Areas most frequently affected
are the optic nerves, chiasm, and tracts; the cerebrum; the brain stem & cerebellum;
and spinal cord. Ø Eventually, the axons themselves begin to degenerate, resulting in
permanent & irreversible damage. Clinical Manifestations Ø Benign course
& symptoms are so mild that the pt. does not seek health care or treatment Ø
Primary progressive MS may result in quadriparesis, cognitive dysfunction, visual loss &
brain stem syndromes. Ø Primary symptoms: fatigue, depression, weakness,
numbness, difficulty in coordination, loss of balance, & pain. Ø 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. Ø
Fatigue is defined as a subjective lack of physical or mental energy that interferes w/ desired
activity. Ø Depression, heat, anemia, deconditioning & medication may
contribute to fatigue. Ø Avoiding heat temperatures, effective treatment of depression
& anemia, and physical therapy my control fatigue. Ø Lesions on the sensory
pathways cause pain. Ø Additional sensory manifestations: paresthesias,
dysesthesias & propprioception loss. Ø Spasticity (muscle hypertonicity) of the
extremities and loss of the abdominal reflexes result from involvement of the main motor
pathways (pyramidal tracts) of the spinal cord. Ø Disruption of the sensory axons may
produce sensory dysfunction (paresthesias, pain). Ø Cognitive & psychosocial
problems may reflect frontal or parietal lobe involvement. Ø Involvement of the
cerebellum or basal ganglia can produce ataxia (impaired coordination of movements) and
tremor. Ø Loss of control connections between the cortex and the basal ganglia may
occur and cause emotional lability and euphoria. Ø Bladder, bowel and sexual
dysfunctions are common. Ø Secondary complications: UTI, constipation, pressure
ulcers, contracture deformities, dependent pedal edema, pneumonia, reactive depression
& decreased bone density. Ø Exacerbations & remissions are
characteristics of MS. o Exacerbations: new symptoms appear and existing ones worsen o
Remission: symptoms decrease or disappear. Glossary Ø Agnosias: loss of ability to
recognize objects through a particular sensory system; may be visual, auditory or tactile.
Ø Akathesia: restlessness, urgent need to move around, and agitation Ø
Akinetic Mutism: unresponsiveness to the environment; the patient makes no movement or
sound but sometimes opens the eye Ø Altered level of consciousness: condition of
being less responsive to & aware of environmental stimuli Ø Aneurysm: a
weakening or bulge in an arterial wall Ø Aphasia: inability to express oneself or to
understand language Ø Apraxia: inability to performed previously learned purposeful
motor acts on a voluntary basis Ø Ataxia: impaired ability to coordinate movement,
often seen as a staggering gait or postural imbalance Ø Autonomic dysreflexia: a life
threatening emergency in spinal cord injury pr that causes a hypertensive emergency; also
called autonomic hyperreflexia Ø Autoregulation: ability of cerebral blood vessels to
dilate or constrict to maintain stable cerebral blood flow despite changes in systemic arterial
BP Ø Autonomic nervous system: division of nervous system that regulates the
involuntary body functions. Ø Axon: portion of neuron that conducts impulses away
from the cell body. Ø Babiski reflex (sign): a reflex action of the toes; indicative of
abnormalities in the motor control pathways leading form the cerebral cortex. Ø
Bradykinesia: very slow voluntary movements and speech Ø Brain injury: an injury to
the skull or brain that is severe enough to interfere w/ normal functioning Ø 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 Ø 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 Ø
Brain death: irreversible loss of all functions of the entire brain, including brain stem Ø
Bulbar paralysis: immobility of muscles innervated by cranial nerves w/ their cell bodies in the
lower portion of the brain stem Ø Chorea: rapid, jerky, involuntary, purposeless
movement of the extremities or facial muscles, including facial grimace Ø Clonus:
abnormal movement marked by alternating contraction and relaxation of a muscle occurring
in rapid succession. Ø Coma: prolonged state of unconsciousness Ø
Complete spinal cord lesion: a condition involves total loss of sensation and voluntary muscle
control below the lesion Ø Concussion: a temporary loss of neurologic function w no
apparent structural damage to the brain Ø Contusion: bruising damage to the brain
surface Ø Craniectomy: a surgical procedure that involves removal of a portion of the
skull Ø Cushing response: brains attempts to restore blood flow by increasing arterial
pressure to overcome the increased intracranial pressure Ø Decerebration: an
abnormal body posture asso w/ a severe brain injury, characterized by extreme extension of
the upper and lower extremities Ø Decortications: an abnormal posture asso w/ a
severe brain injury, characterized by extreme flexion of the upper and lower extremities
Ø Delirium: transient loss of intellectual function, usually due to systemic problems
Ø Dementia: a progressive organic mental disorder characterized by personality
changes, confusion, disorientation, and deterioration of intellect asso w/ impaired memory
and judgement Ø Dendrite: portion of the neuron that conducts impulses toward the
cell body. Ø Diplopia: double vision, or the awareness of two images of the same
objectoccuring in one or both eyes Ø Dsyphagia: difficulty in swallowing, causing the
pt to at risk for aspiration Ø Dysphonia: voice impairment or altered voice production
and incoordination of muscles responsible to speech Ø Dysarthria: defects of
articulation due to neurologic causes Ø Dyskinesias: impaired ability to execute
voluntary movements Ø Epidural monitor: a sensor placed between the skull &
the dura to monitor intracranial pressure Ø Epilepsy: a group of syndromes
characterized by paroxysmal transient disturbances of brain function Ø Expressive
aphasia: inability to express oneself due; often asso w/ damage to the left frontal lobe
Ø Fiberoptic monitor: a system that uses light refraction to determine intracranial
pressure Ø Flaccid: displaying lack of muscle tone, limp, floppy Ø Halo-vest: a
lightweight vest w/ an attached halo that stabilizes the cervical spine Ø Head injury:
an injury to the scalp, skull, and/or brain Ø Hemianopsia: blindness of half, of the field
of vision in one or both eyes Ø 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 Ø
Hernation: abnormal protrusion of tissue through a defect or natural opening Ø
Incomplete spinal cord lesion: a condition where there is preservation of the sensory or motor
fibers, or both, below the lesion Ø Infarction: a zone of tissue deprived of blood
supply Ø Intracranial pressure: pressure exerted by the vol. of the intracranial
contents w/in the cranial vault Ø Korsakoff’s syndrome: personality disorder
characterized by psychosis, disorientation, delirium, insomnia & hallucination Ø
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. Ø 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 Ø Micrographia: small and often illegible
handwrtting Ø Migraine headache: a severe, unrelenting headache often
accompanied by symptoms such as nausea, vomiting and visual disturbances Ø
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 Ø 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 Ø Neurodegenerative: a dse, or condtion that leads to deterioration of
normal clees or function of the nervous system Ø Neuropathy: general term indicating
a disorder of the nervous system Ø Papilledema: edema of the optic nerve Ø
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 Ø Parasympathetic
nervous system: division of the ANS active primarily during nonstressful conditions,
controlling mostly visceral functions. Ø Paresthesias: a sensation numbness or
tingling or a “pins” and “needles” sensation Ø Penumbra
region: area of flow cerebral blood flow Ø Persistent vegetative state: condition in w/c
the pt is wakeful but devoid of conscious content, w/out cognitive or affective mental function
Ø Photophobia: inability to tolerate light Ø Position (postural) sense:
awareness of position of parts of the body w/out looking at them, also referred to as
proprioception Ø Primary headache: a headache for w/c no specific organic cause
can be found Ø Prion: a particle smaller than a virus that is resistant to standard
sterilization procedures Ø Radioculopathy: dse of spinal nerve root, often resulting in
pain and extreme sensitivity to touch Ø Reflex: an automatic response stimuli
Ø Receptive aphasia: inability to understand what someone else is saying; often asso
w/ damage to the temporal area Ø Rigidity: increase in muscle tone at rest
characterized by increased resistance to passive stretch. Ø 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.
Ø Sciatica: inflammation of sciatic nerve, resulting in pain and tenderness along the
nerve through the thigh and leg Ø Secondary headache: headache identified as a
symptom of another organic disorder Ø Secondary injury: an insult to the brain
subsequent to the original traumatic event Ø Seizures: paroxysmal transient
disturbance of the brain resulting from a discharge of abnormal electrical activity Ø
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 Ø Spinal cord injury: an
injury to the spinal cord, vertebral column, supporting soft tissue or intervertebral disk caused
by trauma Ø Spondylosis: ankylosis or stiffening if the cervical or lumbar vertebrae
Ø Spongiform: having the appearance or quality of a sponge Ø Status
epilepticus: episode in w/c the pt. experiences multiple seizure bursts w/ no recovery time
between Ø Sunarachnoid screw or bolt: device placed into the subarachnoid space to
measure intracranial pressure Ø Sympathetic Nervous System: division of the ANS
w/ predominantly excitatory responses, the “fight-or-flight” system Ø
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 Ø Tone: tension
present in a muscle at rest Ø Transaction: severing of the spinal cord itself;
transaction can be complete (all the way through the cord) or incomplete (partially through)
Ø Transsphenoidal: surgical approach to the pituitary via the sphenoid sinuses
Ø Ventriculostomy: a catheter placed in one lateral ventricles of the brain to measure
intracranial pressure and allow for drainage of fluid Ø Vertigo: an illusion of
movement, usually rotation DOWNLOAD