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Perception and More than 10 minutes of oxygen deprivation-brain death

White matter-less perfusion (bundles of fibers, terminal ends)


Coordination Gray matter-more perfusion (body of neurons)

Sources of Blood supply:


Perception-conscious recognition and interpretation 1. Internal carotid arteries-anterior circulation,
(awareness) of the sensory stimuli that serve as a basis for ipsilateral hemispheres
understanding, learning and knowing or for the motivation of 2. Vertebral arteries-posterior circulation, posterior
a particular action or reaction fossa

Coordination-when action or reaction towards a •Circle of Willis


stimulus is occurring in a purposeful, orderly fashion, • act as a safety valve; arises from basilar
appropriate response to a stimulus
arteries and internal carotid arteries;
vascular network at the base of the brain
Role of Nervous System:
• is important to total brain circulation
1. Reciprocally interact with the environment
because it provides equal circulation
2. Maintain homeostasis (with the endocrine system)
bilaterally. If one side of the circle of
Willis is unable to supply adequate
Function:
blood, the other side provides blood to
1. Sensory-interpret incoming message
the area normally supplied by the
2. Integrative-analyze, store, make decisions regarding
damaged side (Phipps, 1998, p. 1892)
appropriate behavior
3. Motor-initiating muscular or glandular activity;
ongoing and evolving interaction with environment •Cerebral arteries (2 each):
Anterior, Middle, Posterior
Ventricles and CSF •Jugular veins-drains the brain venous blood through
• Ventricles- four fluid-filled cavities within the brain dural sinuses
that connect one another and with the spinal canal
• CSF- form in the choroids plexus; about 135 cc
Special characteristics of Cerebral Perfusion
1. Autoregulation
o Cushions
o Provide nutrients • 3 Physiologic mechanisms under normal
o Allow fluid shifts circumstances:
o Changes in intracranial pressure
3 essential components of skull: o Cerebral vasodilation
1. Brain tissue-78% o Metabolic factors
2. Blood -12 %
3. CSF-10% • Mean arterial pressure at which autoregulation is
effective (70-105 mmHg)
-Upper limit is 150 mmHg
Monro-Kellie Hypothesis
If volume added to the cranial vault equals the MAP= SBP + 2 (DBP)
volume displaced from it, the total intracranial volume 3
will not change SBP-Systolic blood pressure
Normal ICP: 60-150 mmH20 or 0-15 mmHg DBP-Diastolic blood pressure
• Cerebral perfusion pressure needed to ensure
blood flow to the brain
CPP=MAP-ICP
Normal Compensatory Adaptations:
Initial: • As CPP decreases, autoregulation fails and CBF
o Increases CSF absorption diminishes
-30 mmHg is incompatible with life
o Displacement of CSF into the spinal subarachnoid
space—space between arachnoid and pia mater) 2. Blood brain barrier
o Collapse of the cerebral veins and dural sinuses • physiologic barrier between blood
capillaries and brain tissue
Other mechanisms:
o Distensibility of the dura
o Increased venous outflow
o Decreased CSF production
o Constriction and vasodilation
o Slight compression of brain tissue NEUROPHYSIOLOGY
Cerebral Blood Flow Neurotransmission-conduction of an impulse
• Amount of blood in milliliters passing
throughout the nervous system
through 100g of brain tissue in 1 minute
• Global CBF-approximately 50 ml/min
Neurons
• Brain needs constant supply of oxygen and
• Receive and transmit impulses; non-mitotic
glucose (20% of body’s oxygen, 25% of
• Excitable, conductive and can influence other cells
body’s glucose)
• Parts: cell body (soma), dendrites (short) and Cranium and Cerebral column
axon • Cranium-composed of 8 cranial and facial bones
• Myelinated and unmyelinated • Foramen magnum-largest hole through which
the brain stem extends to the spinal cord
Note: • Vertebral column-protects the spinal cord,
When injured, centrally located neurons are unable to supports the head and provides flexibility;
reproduce themselves because most cell bodies are located strengthened by ligaments and fibrocartilage
centrally and nerve cell bodies cannot reproduce. However, disc
nerve endings can regenerate (Phipps, 1998, p. 1887).

I. Transmission within the Nerve fiber


Cranial meninges
Action potential
• Dura mater
• Chemical gradient • Arachnoid
• Electrical gradient • Pia mater
Propagation of Action Potential
1. Resting stage (positive outside, negative Falx cerebri-divides the left from right hemispheres
inside) Subdural-more bleeding
2. Depolarization phase (negative outside,
positive inside)

II. Transmission across Synapse Central Nervous system:


Synapses-small gaps between neurons I. Cerebrum
• Chemical or electrical a. Consists of 2 hemisphere
b. Corpus callosum-connects two hemisphere
• One-way junction
c. Cerebral cortex-outer surface of the cerebrum
1. Impulses reaches the presynaptic d. Basal ganglia-located deep within cerebral
terminal hemisphere
2. Vesicles release neurotransmitters e. Internal capsule-white matter consisting of
3. Neurotransmitters inactivated to bundle of nerve fibers carrying motor and
prevent sustained response sensory impulses to and from cerebral cortex

Neurotransmitters-can be excitatory or inhibitory)


Types: Lobes of the Cerebrum and their Functions
1. Acetylcholine-muscle movement
2. Biogenic amines (thinking process) Area Functions
-Dopamine -Serotonin Frontal Controls movements of
-Norepinephrine -Histamine voluntary muscle
3. Amino acids
Primary motor area Facilitates voluntary
-GABA
movement of skeletal
-Peptides
muscle
Speech area (Wernick’s ) Understanding of spoken
Neuroglia-protect and nourish neurons; mitotic
- Located in the and written words
- do not transmit impulses
posterior part of the
Neuroglia Function superior temporal
Astrocytes Supply nutrients to neurons convolution
Microglia Provide protection against Motor area (Broca’s) Promotes vocalization of
microorganisms - Located in the lateral, words
Oligodendrocytes Wrap tightly around nerve inferior portion of the
fibers to form myelin sheath frontal lobe
Ependymal cells Ciliated; line brain cavities; Temporal Receives and interpret
forms CSF olfactory and auditory
Schwann cells Phagocytic cells that form stimuli
myelin sheath around nerve Parietal Promotes recognition of
fibers pain, coldness, light touch
Satellite cells Found in the PNS; may (Contralateral reception)
maintain chemical balance of Occipital Receives and interprets
neurons visual stimuli

II. Diencephalon
• Embedded in the brain superior to brain stem
• Thalamus-process sensory impulses before it
reaches cerebral cortex
• Hypothalamus-regulates endocrine and
autonomic function, temperature, water
metabolism, appetite, emotion, sleep-wake cycle
and thirst
• Epithalamus-includes pineal gland (secretes
melatonin and inhibits LH), part of endocrine
system, affects growth and development.

III. Brain Stem


• Midbrain-center for auditory and visual reflexes • Dermatomes-area of the skin
• Pons-contains the fiber tracts; contains nuclei innervated by cutaneous branches
that controls respiration of a single spinal nerve
-contains pneumotaxic center—controls
rhythmic quality of respirations
• Medulla-control cardiac rate, BP, respirators and
Somatic Nervous system
• Consists of motor and sensory nerves
swallowing
• Reticular activating system (RAS)-influence • Controls skeletal muscles
excitatory and inhibitory control of motor • Produces a motor response through
neuron; regulatory system for consciousness efficient nerve fibers from CNS which
transmit impulses to the skin and
skeletal muscles
IV. Cerebellum
• Has two hemispheres Autonomic Nervous System
• Coordination of skeletal muscle activity, • Controls involuntary or automatic body functions
maintenance of balance, posture and control of • Has two subdivisions, serving same organ but have
voluntary movements counterbalancing effects; each system can inhibit the
organ stimulated by the other

V. Spinal cord
• Sympathetic Nervous System
• Extends from medulla up to first lumbar
 originates from lateral horns of first
vertebra
thoracic through the first lumbar of
• Gives rise to 31 pairs of spiral nerves (C1-
spinal cord (thoracolumbar)
C8, T1-T12, L1-L5, S1-S5, coccygeal nerve)  helps the body cope with events in the
• Center for conducting messages to and from external environment
the brain; a reflex center  Functions mainly during stress,
triggering the fight or flight response
Divisions:  Increases heart rate and respiratory
rate, pupil dilation, cold, and sweaty
Ascending (Spinocerebellar) palms
• Carry a specific sensory information to
higher levels of CNS
• Parasympathetic Nervous System
• Spinocerebellar tracts-muscle tension and
 Consist of the vagus nerves originating
body position
in the medulla of the brain stem and
• Spinothalamic-pain and temperature
spinal nerves originating from the
sensation
sacral region of the spinal cord
(craniosacral)
Descending (Corticospinal)
 Activates GI system
• Pyramidal tracts-from the cortex to cranial
 Supports restorative, resting body
and peripheral nerves; inhibits muscle tone
function through such actions as
• Extrapyramidal tracts-from brain stem,
replenishing fluids and electrolytes
basal ganglia, and cerebellum; maintains
muscle tone and gross body movements
Effect organ Sympathetic Parasympathetic
• Upper motor neurons-from cerebral cortex
Heart Increased rate Decreased rate
to anterior gray column of SC; spasticity
and contractility and contractility
and hyperactive reflexes
Lungs Relaxation Contraction
• Lower motor neurons-“final common
GIT
pathways” from anterior gray column up to
• Motility Decreased Increased
muscles; flaccidity and loss of reflexes
• Tone Contraction Relaxation
VI. Reflex arc sphincter
s
• Reflexes-automatic action; spinal cord
Urinary bladder
mediates most reflexes
• Bladder Relaxation Contraction
• Automatic or perceptible, inhibited or
muscle
conditioned
• Sphincter Contraction Relaxation
• Hyperreflexia-disease or injury of Liver Glycogenolysis None
certain descending motor tracts
• Hyporeflexia-damage or
degeneration of the sensory or
Sensory System (General and special)
motor neurons
Type of receptors:
1. Exteroreceptors
Peripheral Nervous system 2. Interoreceptors
• Cranial nerves-innervate head and neck 3. Proprioceptors-specific receptors to detect balance,
region, except the vagus nerve sense of position
• Spinal nerves 4. Mechanoceptors-detect pressure, touch (any
• Plexuses-complex cluster of nerve stimulus that is physical in nature)
fibers (cervical, brachial, lumbar 5. Thermoreceptors-any changes in temperature
and sacral region) 6. Photoreceptors-light stimulus
7. Chemoreceptors-taste, olfactory, pancreatic enzymes
8. Nociceptors-severe stimulus
9. Cutaneous receptors-touch
• Loudness- Neurologic or psychologic
Special senses: interpretation of intensity; the greater
• Sense of Sight intensity of the sound waves stimulating
the organ of Corti, the greater will be
• Collect light waves and transmit them as the size of nerve impulses
impulses to the brain, which translate
them into images Decibels(dB)-unit of measure of intensity of sound
• Normally form of a clear retinal image of Normal conversation= 65 dB
an object at 20 ft. away Amplified rock music= 120 dB
• Binocular vision—ability to judge relative, Nearby jetplane= about 140 dB
distances of objects
Pitch
Anatomical features of the Eyeball •Corresponds to frequency; the higher the
Outer: frequency the higher the pitch of the sound
1. Cornea-thin, tough, transparent layer supplied •Humans can potentially hear sounds whose
with sensory nerve (touch and pain), no blood frequency range from 16 to 2000 Hz
supply, oxygen and glucose through diffusion •Upper range decreases slight with increasing age
2. Sclera •Speech falls in the range of 85-1050 Hz

Middle: Physiology of Hearing


1. Choroid –highly vascular, dark brown membrane 1. Sound waves moving through the air enter the canal
2. Ciliary body-contract and dilate ciliary process and move down to it to strike against the tympanic
which contain capillaries that secrete fluid membrane causing it to vibrate
3. Iris-visible colored part of the eye; controls pupil 2. Vibrations of the tympanic membrane move the
size malleus

Inner:
3. Movement of the malleus to the incus
1. Retina-neural tissue, phagocytic, stores Vit. A, 4. As the incus moves, it moves the stapes against the
contains rods and cones oval window, it starts a ripple on the perilymph
2. Fovea-responsible for highly colored vision 5. Movement of the perilymph is transmitted to the
endolymph muscle inside the cochlear duct and
Refraction stimulates the organ of Corti
• bending of light when it meets surfaces of 6. Cochlear nerve conduct impulses from the organ of
different medium Corti to the brain; hearing occurs when impulses
reaches auditory area in the temporal lobe of
cerebral cortex
Refractory media of the Eye
1. Cornea-performs most of the refraction because of
its convex form
2. Aqueous humor-fluid at the anterior and posterior
Mental Status Examination
chamber of the anterior cavity • An indication of how patient is functioning as a whole
3. Crystalline lens-greatest refractive power and how the patient is adapting to the environment
4. Vitrous humor- thick, gelatinous fluid found at 1. General appearance
posterior chamber, give spherical shape to the eye 2. State of consciousness
• Arousal component
Physiology of Vision • Content component
Formation of an image on the retina accomplished by the 3. Mood and effect-changes in the nervous system
following: 4. Thought content
1. Refraction 5. Intellectual capacity
2. Accomodation
3. Constriction of pupils NEUROLOGIC ASSESSMENT
4. Convergence of eyeballs I. Comprehensive History Taking
• Demographic Data
Stimulation of retina • Current health
•Dim light causes breakdown of the chemical • Past health history
rhodopsin present in rods
• Medication history
•Cones-responsible for daylight and color vision
•Perception of color is dependent on the cones • Growth and development
•Most cones concentrated on fovea centralis • Family health history
•Condition to central area in occipital lobe • Psychosocial history
II. V/S
• Sense of Hearing III. Mental Status Assessment
Parts of the ear • LOC
1. Outer-collects sound • Orientation
2. Inner-conducts sound • Memory
•Eustachian tube • Mood/affect
• joins the middle ear and nasopharynx • Intellectual performance
• transmit sound waves and maintain • Judgment/Insight
equilibrium • Language/communication

Interpretation of sound
IV. Motor System assessment-muscle strength,
tone, coordination, gait and station movement
• Cranial nerve III, IV, VI (Oculomotor, Trochlear,
V. Sensory Function-superficial sensation, Abducens)-motor nerves that arise from the brainstem
touch/pain, temperature, proprioception, 1. Nystagmus –- involuntary eye movement;
discrimination strokes of anterior, inferior, superior,
VI. Reflex activity cerebellar arteries
VII. Cranial nerve testing 2. Constricted pupils: may signify impaired
blood flow to vertebralbasilar arteries.
3. Ptosis (eyelid falldown); dropping of the
MENTAL STATUS ASSESSMENT WITH ABNORMAL upper eyelid over the globe—strokes of
FINDINGS posterior inferior cerebellar artery;
myasthenia gravis, palsy of CN III

• Unilateral neglect (lack of caring of the other side of the


• Cranial nerve V (Trigeminal)—largest cranial nerve with
body); strokes involving middle cerebral artery.
motor and sensory components: changes in facial
sensations; impaired blood flow to carotid artery
• Poor hygiene and grooming: dementing disorders 1. Decreased sensation of face and cornea on same
• Abnormal gait and posture: transient ischemic side of body; strokes of posterior inferior cerebral
attacks(TIAs) , strokes, and Parkinson’s disease artery
2. Lip and mouth numbness
• Emotional swings, personality changes: strokes
3. Loss of facial sensation: contraction of masseter and
• Aphasia-defective or absent language function: TIA’s, temporal muscles, lesions CN V
strokes involving anterior/posterior artery; general term 4. Severe facial pain: trigeminal neuralgia (tic
for impairment of language dorlourex)
• Dysphonia- change in tone of voice
• Cranial VII (Facial nerve)—mixed nerve concerned with
• Dysarthria- (different in speaking); is indistinctness of
facial movement and sensation of taste
words in word articulation resulting from interference 1. Loss of ability to taste
with the peripheral speech mechanisms (e.g. muscles of 2. Decreased movement of facial muscles
the tongue, palate, pharynx, or lips) [Phipps, 1998, p.
1901]
3. Inability to close eyes, flat nasolabial fold, paralysis
• Decreased level of consciousness of lower face, inability to wrinkle the forehead
• Confusion, Coma 4. Eyelid weakness; paralysis of lower face; paralysis of
upper motor neuron
5. Pain, paralysis, sagging of facial muscles: affected
COGNITIVE FUNCTION ASSESSMENT WITH side in Bell’s palsy
ABNORMAL FINDINGS
• Cranial VIII (Acoustic)—composed of a cochlear division
• Disorientation to time and place: stroke of right cerebral related to hearing and a vestibular division related to
equilibrium (Phipps, 1998, p. 1909)
hemisphere
• Decreased hearing or deafness: strokes of
1. Memory deficits
vertebralbasilar arteries or tumors of CN VIII
2. Emotional defense
• Cranial IX(Glossopharyngeal) and cranial X (Vagus)—
CRANIAL NERVE ASSESSMENTS chief function of cranial nerve IX is sensory to the
• Cranial I (Olfactory): Anosmia pharynx and taste to the posterior third of tongue;
cranial nerve X is the chief motor nerve to the soft
1. lesions of frontal lobes
palatal, pharyngeal and laryngeal muscles (Phipps, 1998,
2. impaired blood flow to middle cerebral
p. 1909)
artery.
1. Dysphagia (difficulty swallowing)
2. Unilateral loss of gag reflex
• Cranial II (Optic)
• Cranial XI (Spinal accessory)—motor nerve that supplies
1. blindness in eye: strokes of internal carotid
the sternocleidomastoid muscle and upper part of
artery, TIA’s
trapezius muscles
2. Homonymous hemianopia - impaired vision 1. Muscle weakness
or blindness in one side of both eyes; 2. Cortralateral hemiparesis: strokes affecting middle
blockage of posterior cerebral artery. cerebral artery and internal artery
3. Impaired vision: strokes of anterior cerebral • Cranial XII (Hypoglossal)
artery; brain tumors 1. Atrophy, fasciculations (twitches): LMN disease
Note: 2. Tongue deviation toward involved side of the body
• Visual acquity-mediated by the cones of the
retina
SENSORY FUNCTION ASSESSMENT WITH
• Field of vision or peripheral vision-portion of
ABNORMAL FINDINGS
space in which objects are visible during the • Altered sensation occurs with variety of neurologic
fixation of vision in one direction. The pathology
receptors for peripheral fields are the rod • Altered sense of position: lesions of posterior
neurons of the retina. (Phipps, 1998, p.
column of spinal cord
1906)
• Inability to discriminate fine touch: injury to
posterior columns
MOTOR FUNCTION ASSESSMENT WITH
ABNORMAL FINDINGS
• Muscle atrophy: LMNs disease
• Tremors (groups, large of muscle fibers)-
Parkinson’s disease (tremors at rest), multiple
sclerosis (tremors observed in activity) • Positive Kernig’s sign-excessive pain when examiner
attempts to straighten knees with client supine and
• Fasciculations (single muscle fiber): disease or
knees and hips flexed
trauma to LMN, side effects of medications, fever,
sodium deficiency, anemia
• Flaccidity (decreased muscle tone): disease or
trauma to LMN and early stroke
• Spasticity (increased muscle tone): disease of
corticospinal motor tract
• Muscle rigidity: disease of EP motor tract
• Cogwheel rigidity (muscular movement with small
regular jerky movement; parkinson’s disease
• Muscle weakness-in arms, legs, hands: TIAs
• Hemiplegia-paralysis of half of body vertically
• Flaccid paralysis: strokes of anterior spinal artery,
• Decorticate posturing (up)
multiple sclerosis or myasthenia gravis
• Total loss of motor function: below level of injury
• Spasticity of muscle: incomplete cord injuries

CEREBELLAR FUNCTION ASSESSMENT WITH


ABNORMAL FINDINGS
• Ataxia (lack of coordination and clumsiness of
movement, staggering, wide-based and
unbalanced gait) • Decerebrate posturing (down)

• Steppage gait (client drags or lifts foot high, then


slaps foot onto floor; inability to walk on heels;
disease of LMN #Altered Level of consciousness
• Sensory ataxia (client walks on heels before 1. Consciousness
bringing down toes and feet are held wide apart; Requires:
gait worsens with eyes closed 1. Arousal: alertness; dependent upon
reticular activating system (RAS); system of
• Parkinsonian gait (stooped over position while neurons in thalamus and upper brain stem
walking with shuffling gait with arms held close to 2. Cognition: complex process, involving all
the side) mental activities; controlled by cerebral
• Romberg’s test (Positive)- With feet approximated, hemispheres
the patient stands with eyes open and then closed;
Process that affect LOC:
if closing the eyes increases the unsteadiness, a
a. Increased ICP
loss of proprioceptive control is indicated
b. Stroke, hematoma, intracranial hemorrhage
c. Tumors
REFLEX d. Infections
• Hyperactive: reflexes e. Demyelinating disorders
• Decreased reflexes
• Clonus of foot (Hyperactive, rhythmic dorsiflexion Systemic Conditions affecting LOC
and plantar flexion of foot)  Hypoglycemia
• Superficial reflexes (such as abdominal) and  F/E imbalance
cremasteric reflex  Accumulated waste products from liver or
• Positive Babinski reflex (dorsiflexion of big toe) renal failure
 Drugs affecting CNS: alcohol, analgesics,
anesthetics
 Seizure activity: exhausts energy
Special Neurologic Assessment metabolites
 Level of Consciousness
• Brudzinski’s sign (pain, resistance, flexion of hips • Alert
and knees when head flexed to chest with client • Lethargic-very sleepy
supine) • Obtunded
• Stuporous
• Coma
• Death

Client Assessment with Decreased LOC


a. Increased stimulation required to elicit response
from client
b. More difficult to arouse; client agitated and confused • Eyes may wander but cannot track objects
when awakened • Minimally conscious state: client aware of
c. Orientation changes: losses orientation to time first, environment, can follow simple commands,
then place, person indicates yes/no responses; make meaningful
d. Continuous stimulation required to maintain movements (blink, smile)
wakefulness • Often results from severe head injury or global
e. Client has no response, even to painful stimulation anoxia

Loss of Simultaneous Eye Movement


Loss of normal reflex functioning: Locked-in syndrome
1. Doll’s eye movement: eye movement in opposite 1. Client is alert and fully aware of environment; intact
direction of head rotation (normal function of brain cognitive abilities but unable to communicate
stem) through speech or movement because of blocked
2. Oculocephalic reflex: eye move upward with passive efferent pathways from brain
flexion of neck; downward with passive neck 2. Motor paralysis but cranial nerves may be intact
extension (normal function) allowing client to communicate through eye
3. Oculovestibular response (cold caloric testing): movement and blinking
instillation of cold water in ear canal cause
nystagmus (lateral tonic deviation of eyes) toward
3. Occurs with hemorrhage or infarction of pons,
stimulus (normal function) disorders of lower motor neurons or muscles

Brain Death
GLASGOW RESPONSE
1. Cessation and irreversibility of all brain functions
Eye opening responses
4 Opens eyes spontaneously 2. General criteria:
3 Opens eyes in a. Absent motor and reflex movements
response to voice 2 Opens eye in b. Apnea
response to painful stimuli 1 Does not c. Fixed and dilated pupils
open eyes d. No ocular responses to head turning and caloric
Best verbal response stimulation
5 Oriented e. Flat EEG
4 Confused
3 Utters inappropriate words NURSING DIAGNOSIS
2 Incomprehensible words • Ineffective airway clearance: limit
1 None suctioning to <10-15 seconds,
hyperoxygenate
• Risk for aspiration
• Risk for impaired skin integrity: preventive
measures, continual inspection
• Impaired physical mobility: maintain
B functionality of joints, physical therapy
est • Risk for Imbalanced Nutrition: Less than
motor response body requirements
6 Obeys command • Anxiety (of family)
5 Localizes pain
4 Withdraws with painful stimuli
3 Flexion (Decorticate posturing) ICP
2 Extension (Decerebrate posturing  Increased blood volume, increased brain volume,
1 None increased CSF volume
Total 3-15  Normal pressure: 5-15 mmHg, with pressure
14 – no impairment tranducer with head elevated 30˚; 60-180 cmH20,
3 – compatible with brain death water manometer with client lateral recumbent
7 – state of coma  Sustained increases associated with:
a. Cerebral edema
MOTOR FUNCTION ASSESSMENT b. Head trauma
a. Client follows verbal commands c. Tumors
b. Pushes away purposely from noxious stimuli d. Abscesses
e. Stroke
c. Movements are more generalized and less purposeful
f. Inflammation
(withdrawal, grimacing) g. Hemorrhage
d. Reflexive motor responses
e. Flaccid with little or no motor response
 Factors that Increases ICP
• Hypercapnea, hypoxemia
COMA • Cerebral vasodilating agents
• Valsalva maneuver; coughing or sneezing
Irreversible coma - vegetative state • Body positioning (prone, neck flexion,
• Permanent condition of complete unawareness extreme hip flexion)
of self and environment, death of cerebral • Isometric muscle contraction
hemispheres with continued function of brain • Emotional upset; noxious stimuli
stem and cerebellum • Arousal from sleep
• Client does not respond meaningfully to • Clustering of activities
environment but has sleep-wake cycles and • Pain and agitation
retains ability to chew, swallow and cough
ICP 2. Risk for infection: open head wounds and intracranial
monitor device requires meticulous aseptic technique
Cranial insult Tissue edema Increased ICP 3. Anxiety (family)

Compression of blood vessels

Decreased cerebral blood flow Client with Seizure Disorder


Seizures-alteration in consciousness, sensory and motor
Decreased oxygen with brain cell death • Paroxysmal motor, sensory, or cognitive
manifestations of spontaneous abnormal
Edema around necrotic tissue discharges from neurons in cerebral cortex
• May involve all or part of brain consciousness,
Increased ICP with brainstem and respiratory center autonomic function, motor function and
compression sensation

Carbon dioxide accumulation Epilepsy: any disorder characterized by recurrent seizures

Vasodilation Increased ICP DEATH


Categorization of seizures:
Partial seizures: activation of part of one cerebral
Pathophysiology: pressure results to lack of oxygen and hemisphere
a. Simple partial seizure: no altered consciousness,
blood supply
recurrent muscle contraction; motor portion of
cortex affected
Manifestations:
• Decreasing level of sensorium-most sensitive,
reliable and earliest indicator: due to cerebral b. Complex partial seizure: impaired
hypoxia, interference with RAS function consciousness; may engage in automatisms
• Increasing BP, decreasing pulse (repetitive nonpurposeful activity such as lip
• Pupillary changes (a reflection of tissue shifts smacking, preceded by aura, originates in the
• Cushing’s triad-increasing systolic pressure, temporal lobe)
widening pulse pressure and bradycardia (final
compensatory mechanism to maintain CSF) Generalized seizures:
• Papilledema-due to the compression of optic disc  Involves both brain hemispheres;
• Respiratory changes-dependent on site of consciousness always impaired
pressure  Absence seizures (petit mal): characterized
• Motor changes-dependent on site of pressure; by sudden brief cessation of all motor
usually starts contralaterally; then hemiplegia, activity, blank stare and unresponsiveness
decortication or decerebation depending on often with eyes fluttering
pressure on brain stem
Tonic-clonic seizures
Late signs: coma, apnea, unilateral pupil changes  Preceded by aura, sudden loss of
consciousness
Medications for Increased ICP  Tonic phase: rigid muscles, incontinence (as
• Osmotic diuretics increases osmolarity of blood and muscle contracts, bladder relax)
draw fluid from edematous brain and tissue into  Clonic phase: altered contraction,
vascular bed relaxation, eyes roll back, froths at mouth
• Loop diuretics such as furosemide  Post-ictal phase: unconscious and
• Antipyretics or hypothermia blanket: used to control unresponsive to stimuli
increases in cerebral metabolic rate
• Anticonvulsants to manage seizure activity State Epilepticus
• Histamine H2 receptors to decrease risk of stress 1. Continuous seizure activity, generally tonic-clonic
ulcers type
• Barbiturates: may be given as continuous infusion to 2. Client at risk to develop hypoxia, acidosis,
induce coma and decrease metabolic demands of hypoglycemia, hyperthermia, exhaustion
injured brain 3. Life threatening medical emergency requiring
• Vasoactive medicine may be given to maintain blood immediate treatment:
pressure to cerebral perfusion a. Establish and maintain airway
b. Diazepam (Valium) and Lorazepam (Ativan)
Surgery-include removal of brain tumors, burr holes, insertion intravenously at
of drainage catheter or shunt to drain excessive CSF c. 50% Dextrose IV
d. Phenytoin (Dilantin) IV-increase seizure threshold
e. Pentobarbital-lessen nervous irritation
ICP monitoring
• Continuous intracranial pressure monitor is used for Medications:
continual assessment of ICP and to monitor effects a. Manage but do not cure seizures
of medical therapy and nursing interventions b. Raise seizure threshold
• Risk of infection exists with invasive procedure c. Carbamezepine
d. Phentoin
Nursing Diagnosis e. Valproic acid
1. Ineffective Tissue perfusion
Key Interventions:
1. Proper client from injury and maintaining airway Dilate blood vessels
2. Do not force anything into the client’s mouth
3. Loosen clothing around neck Pressure on nerves

Nursing Diagnosis: 5. Migraine headache: 1:4 household


1. Risk for Ineffective airway clearance  Women 3x more than men: 3days a week
2. Anxiety  May be caused by:
Light
Interventions: Noise
1. Assess for signs and symptoms of seizure activity Irregular eating and sleep
such as report of aura or twitching of muscle groups Chocolate
2. Have an oral airway oxygen and suction readily Strong smell
available Peanut butter
3. Stay with client to protect him from injury and
observe seizure activity. If he is in bed, remove Electrical impulse altered and triggers trigeminal
pillows, raise side rails, put bed on flat position. nerve
Loosen any restrictive clothing
4. After seizure, assess respiration and pulse. If they Trigeminal nerve=vasodilation and nerve
present and he is unresponsive turn him onto his irritation
side to keep his airway patent
5. Cover him with a blanket for warmth and privacy 6. Cluster Headache
6. Observe and document characteristics of the seizure  Excruciating pain
 6 x more in men, 30 min to 2 hours
Client with Headache Nerves irritated
1. May be due to benign or pathological condition
Pain signals
Pathophysiology: multiple pain sensitive structures within
cranial vault, face, and scalp are stimulated and cause Tension Headache
pain perception
Management:
Types: Pharmacological
Tension-characterized by sensation of tightness around 1. Aspirin, Ibuprofen-suppress prostaglandin that
head and may have specific localized painful areas; areas dilates and sensitize nerve fibers
caused by sustained contraction of muscles and head and 2. Acetaminophen-tension headache; works in CNS to
neck; precipitated by stress and anxiety reduce pain without effect on prostaglandin (safe for
gastritis)
Migraine (more common in women) 3. Triptans-anti-migraine; activates serotonin receptors
- recurring vascular headache often initiated decreasing inflammation of blood vessels
by triggering event and accompanied by 4. Botox (purified botulinum bacteria)
neurologic dysfunction; or increase release - small dosages allow it to be localized;
of sensory substances (e.g. serotonin); paralyses muscles locally and is not
triggers include stress, fluctuating glucose absorbed into the blood stream (may cause
levels, fatigue, hormones, bright lights nerve paralysis if given in large doses)
5. Indomethacin-for cluster headaches; with pain
Cluster (common in men) killers
- typically awakens client with unilateral pain
around eye accompanied by rhinorrhea, Nonpharmacological:
lacrimation, flushing; attacks occur in 1. Biofeedback
clusters of 1-8 days for weeks 2. Acupuncture
3. Massage
HEADACHE 4. Yoga
5. Herbal remedies
1. Tension headache-90% ; noise, stress—sustained
contraction of muscles
2. Sinus Headache
Virus, allergen, bacteria, temp
HEAD INJURY
 Laceration
 Hematoma
Nerves in sinuses swell
 Contussion
 Bleeding
Headache
Sources:
e.g. brain freeze due to swallowing of cold substances
1. Scalp injury
rapidly
2. Skull fracture
3. Brain injury
3. Hang-over headache
Risk factors:
Alcohol blocks hormonal mechanisms
a. Motor vehicle accidents
b. Elevated blood alcohol levels
Dehydration
c. Greatest risk: male aged 15-30 and those over 75
4. Wine headache
Mechanism of trauma:
Increases histamine/tyramine
1. Acceleration injury: head struck by moving
object
2. Deceleration injury: head hits stationary
object
3. Acceleration-deceleration (coup- C. Cerebral edema and Increasesd ICP
countercoup phenomena) head hits objects
and brain rebounds within skull
Skull fracture
Diffuse axonal injury-most severe form of brain injury also • break in continuity of skull usually resulting in
called shearing injury brain trauma
a. Linear: dura remains intact; subdural or epidural
Types of brain Injury: hematoma may occur underneath
a. Open head injuries (dura) b. Comminuted and depressed skull fractures:
b. Closed head injuries –blunt trauma increase risk for direct injury to brain tissue
c. Concussions –caused by sudden blow to the head or from contusion (bruise) and bone fragment: risk
rapid acceleration-deceleration for infection
 results in retrograde amnesia and loss of c. Basilar: involves base of skull (softer) and
consciousness for 5 minutes usually involves extension of adjacent fractures
 No break in skull or dura
 May have headache, nausea or vomiting
d. Contusions-cause more damage, damage to brain Assessment:
itself involve cortical bruising and laceration of • Rhinorrhea: through nose
vessels and brain tissues • Otorrhea: through
• May appear on x-ray
Complications of Brain Injury • Hemotympanum: blood behind
A. Post concussion syndrome: tympanic membrane (purple or dark
Manifestations: color)
 Headache, dizziness Normal: pearly gray
 Nervousness, irritability • Battle’s sign: blood over mastoid
 Changes in intelligence, poor concentrating, process
poor memory • Raccoon eyes: bilateral periorbital
 Fatigability ecchymosis
 Insomia • Glucose reagent strip: If positive
indicates CSF

Traumatic Brain Injury Interventions:


Epidural a. Keep nasopharynx and external ear clean
Subdural
b. No blowing nose, coughing or hard sneezing
Intracerebral
c. Prophylactic antibiotic
B. Hematoma Formation:
Nursing Management for head injuries:
1. Subdural hematoma (slower progression)-
Immediately following surgery:
veins, poor prognosis due to late diagnosis;
• Immobilize head and neck until cervical injury is
occurs within 24-48 hours of injury in acute, 2-
ruled out
14 days in subacute; can occur up to several
• Avoid flexion: hyperextension and rotation of the
months in chronic
neck
• Jaw thrust maneuver
- Patent airway and support ventilatory
Manifestations: function
Acute - Document baseline neurological assessment
• Progressive and marked depression of
consciousness
• Headache, drowsiness, agitation and After initial stabilization:
• Monitor neurological status every hour until stable
confusion
• Pupillary and motor changes - LOC, responsiveness
- Pupillary size, position, direct and
Chronic
consensual response
• Increasing severe headache
- Assess extraocular movements
• Slow cerebration and drowsiness
- Note verbal and motor changes
• Papilledema and ipsilateral pupil dilatation
• Monitor for complications
- Hematoma formation
Systemic-Bilateral
- Infection
2. Epidural (extradural) Hematoma
- Acute hydrocephalus
• Immediate loss of consciousness, lucid - ARDS
interval lasting for few minutes or hours;
lapse into unconsciousness • Monitor temperature and maintain normothermia
• Severe, headache, seizures, vomiting, (decrease metabolism)
hemiparesis, fixed, dilated ipsilateral pupils • Report high urine output (over 200 ml/hr for 2
consecutive hours)
3. Intracerebral Hematoma • Monitor osmolality and serum electrolytes
• Contained well-defined blood clot; usually at • CBC
frontal and temporal lobes • ROM exercises
• Eye/ear care
Management: Craniotomy
• Nutrition-NGT (high glucose-brain functioning; 1. Transient Ischemic attack-brief episodes of
protein-tissue repair) neurologic manifestations which clear completely in
• Elimination-laxatives, increase fiber less than 24 hours
2. Reversible ischemic neurologic deficit-neurologic
Craniotomy-surgical opening of the skull deficits remain after 24 hours but leaves no residual
Craniectomy –permanent removal of the cranium to relieve signs and symptoms after days to weeks
pressure on the brain by providing space for expansion 3. Stroke in-evolution-progressing stroke which
develops over a period of hours or days;
Nursing management manifestations don’t resolve and leave residual
Preoperative neurologic effects
• Parenteral corticosteroids 4. Completed stroke- when neurologic deficits remain
• Scalp preparation unchanged over 2-3 day period
• Antiembolism stockings
Risk Factors
Postoperative • Prior ischemic episodes
1. Neurological assessment •Cardiac disease
2. Head dressings:monitor for CSF leaks •DM
3. Control ICP •Atherosclerotic diseasae
• Assess for signs of increasing ICP •Hypertension, hypercholesterolemia
• Positioning to prevent increase in ICP •Polycythemia
 Supratentorial surgery-elevate •Smoking
head of bed 30 degrees •Oral contraceptives
 Infratentorial-keep flat, turn
•Emotional stress
every 2 hours, but never onto
•Obesity
the back (to prevent brain
hernation) •Family history of stroke
 Posterior fossa surgery-either •Age
side but never on the back
 Bone flap-on the unoperated side Warning signs that may precede CVA
•Paresthesia
•Transient loss of speech
STROKE •Hemiplegia
Stroke is a brain attack
• …needing emergency management, •Severe occipital or nuchal headaches
including specific treatment and secondary •Vertigo or syncope
and tertiary prevention •Motor or sensory disturbances (tingling transient
Stroke is an emergency paralysis)
• …where virtually no allowances for •Epistaxis
worsening are tolerated
Stroke is treatable SPECIFIC DEFICITS
• …optimally, through proven, affordable,
culturally-acceptable and ethical means Dependent upon area damaged
Stroke is preventable •Hemiplegia
• …in implementable ways across all levels of •Aphasia
society - sensory/receptive-Wernick’s aphasia
- motor/expressive-Broca’s aphasia (able to
understand the stimuli but cannot express
Basic Location of Cerebral Aneurysm •Global aphasia
- Agnosia
Cerebral embolus-moving - Dysarthria
Cerebral thrombus - Incontinence
Cerebral hemorrhage - Horner’s syndrome-decrease lacrimation
- Unilateral neglect
Types of strokes
Emotional or Behavioral Reactions:
• Ischemic stroke-little blood flow •Severe mood swings
1. Thrombotic formation of a blood clot with •Social withdrawal
coagulation the results in the narrowing of the
•Inappropriate sexual behavior
lumen of a blood vessel with eventual occlusion
2. Embolic –occlusion of a cerebral artery by an •Outbursts of frustration and/or anger
embolus, resulting in necrosis and edema of the •Regression to an earlier behavior
area supplied by the involved vessel
Right brain damage Left brain damage
• Hemorrhagic stroke-disrupted blood flow •Paralyzed left side •Paralyzed right side
1. Intracerebral hemorrhage stroke-bleeding within •Spatial-perceptual •Impaired speech/language
the brain caused by a rupture of vessels
deficits •Impaired right and left
2. Subarachnoid hemorrhagic stroke-cause by
aneurysm or AV malformation
•Tend to deny or minimize discrimination
problems •Aware of deficits,
Development of CVA •Impaired judgment depression, anxiety
•Impaired time concepts •Impaired comprehension
•Short term span •Slow performance,
cautious

Middle cerebral artery Involvement


SPINAL CORD INJURY
•Contralateral paralysis
•Contralateral anesthesia, loss of proprioception, Manifestations:
fine touch, localization Subjective
•Aphasia •Loss of sensation below level of injury
•Neglect of opposite side •Inability to move
Objectivity
•Homonymous hemianopia-loss of vision for one
half of the visual field
A. Early symptoms of spinal shock
•Absence of reflexes below level of lesion
Diagnostic procedures
•Flaccid paralysis below level of injury
 CT scan-determine if vascular or nonvascular lesions
 Angiography •Hypotonia results in bowel and bladder distention
 MRI •Inability to perspire in affected parts
 Laboratory (CBC, PT, PTT)-not definitive to conform •Hypotension
diagnosis
B. Later symptoms of spinal cord injury
Medical management •Reflex hyperexcitability
 Decreased ICP •State of diminished reflex hyperexcitability below
 BP management site in all instances of cord damage following
 Fluid volume management hyperreflexia
 Tissue plasminogen activator-must be given within 3 •In total cord damage-loss of motor and sensory
hours of onset of manifestations and will dissolve function is permanent
clot; recombinant altephase (Activase rt-pa) •Sacral region-atonic bladder and bowel with
 Antithrombotic (aspirin, clipyridamole)-prevent impairment of sphincter control
platelet aggregation •Lumbar region- spastic bladder and loss of bladder
 Anticoagulant (heparin, clexane) and anal sphincter control
 Steroids or osmotic, diuretics •Thoracic-trunk below the diaphragm
 Antihypertensive and diuretics •Cervical-from neck down, if above C4 respirations
and depressed
Nursing management •In partial cord damage, depends on the type of
 Hourly neurological assessment neurons affected (spastic vs. flaccid)
 Monitor and prevent intracranial hypertension
Clinical manifestations:
•Positioning •Paralysis of muscles of respiration
- bed rest: keep mainly on unaffected side •Bradycardia
- use of pillows to support to prevent flexion •Hypotension
deformity, thrombus formation •Urinary retention
- external hip rotation
- assist in progressive activity (mobility)
•Hypomotility
- Progressive self-care (ADL) •Muscle atrophy
•Poikilothermia-abnormality in sensing change in
•Prevention of injury temperature
- eyes-normal saline, artificial tears, eye
patch
- side rails up
- decubitus ulcer prevention/management MUSCLE FUNCTION AFTER SPINAL CORD
- Oral mucosa care
•Nutrition/prevention of aspiration
INJURY (((log-rolling)
- Communication Spinal Cord Injury Muscle Functioning Muscle Function
- Others: remaining Loss
 Reorientation Cervical, above C4 None All including
 Minimize environmental stimuli respiration
 Emotional support C5 Neck, scapular Arm, chest, all
 Rehabilitative elevation below chest
C6-C7 Neck, some chest Some arm,
•Discharge care
movement, some fingers, some
- Ways to prevent recurrence
arm movement chest movement
 dietary modification
all below chest
 Stress reduction
Thoracic Neck, arms (full), Trunk, all below
 Smoking cessation
some chest chest
 Exercise program
Lumbo-sacral Neck, arms, chest, Legs
 Drug compliance
turnk
- Residual deficits and balancing realistic
expectation
-
-
Special methods of feeding
Ensure continuity of care and emotional
Laminectomy
support Autonomic dysreflexia (after spinal shock resolves)
 Exaggerated autonomic response to stimuli:
such as distended bladder or bowel (e.g. pain)

• Severe hypertension

• Headache
Parkinson’s Disease
(fourth common
• Flushed skin
neurodegenerative disease)
• Diaphoresis • Degeneration of dopamine-providing cells in the
substantia nigra, which leads to degeneration of
• Nasal Congestion neurons in the basal ganglia; usually develops after
60 age
Management
• Associated with decreased levels of dopamine due to
1. Place in high-Fowler’s position
destruction of pigmented neuronal cells in the
2. Ensure patency of urinary drainage and assess substantia nigra in the basal ganglia of the brain
(Smelzer & Bare, 2004, p. 1979)
for infection.

3. Eliminate other potential stimuli • Imbalance between dopamine and acetylcholine

4. Notify physician: administer prescribed


antihypertensive Three cardinal features:
1. Tremors at rest

• e.g. rhythmic, slow turning motion


Nursing Diagnosis
1. Impaired gas exchange related to muscle fatigue (pronation-supination) of the forearm and
and retained secretions. the hand and a motion of the thumb against
the fingers as if rolling a pill
2. Decreased cardiac output r/t venous pooling and
immobility • tremor is present while at rest, increases
when the patient is walking, concentrating,
3. Impaired skin integrity r/t immobility and poor feeling anxious (Smeltzer & Bare, 2004, p.
tissue perfusion 1980).

4. Constipation r/t the injury, inadequate fluid 2. Rigidity-resistance to passive limb movement
intake, diet low in roughage and immobility
3. Bradykinesia-most common features; patients
5. Urinary retention take longer to complete most activities and have
difficulty initiating movement
6. Impaired physical mobility

7. Risk for autonomic dysreflexia r/t reflex Clinical Manifestations:


stimulation of SNS • Generalized feelings of stiffness

8. Altered nutrition less than body requirements r/t • Mild, diffuse muscular pain
increased metabolic demand
• Hand tremor at rest (pill rolling)
9. Sexual dysfunction r/t inability to achieve
erection or perceive pelvic sensations
• Akinesia

• Gait changes –shuffling gait


Medical Management
 Immoblization—Gardner –well tongs, halo
• Characteristic stance-stooped posture
external fixation

 Maintenance of heart rate (Atropine) and BP • Masklike-facial expression


(dopamine) vasopressors
• Speech pattern-slow, low volume monotonous in
 Methylprednisolone therapy tone with poor articulation

 Insertion of NGT • Involuntary drooling

 Intubation, if needed • Decreased lacrimation; constipation,


incontinence
 Indwelling urinary catheter
• Heat intolerance; excessive perspiration
 Stress ulcer prophylaxis (Proton-pump
inhibitos, H2 blockers) • Lack of spontaneous swallowing

 Physical therapy
Medical Management
• Levodopa-Carbidopa T-synthetic precursor of • Believed to be due to reduced acetylcholine
dopamine for basal ganglia (Sinemet) receptors due to destruction and blockage attributed
to autoimmune process
• Anticholinergic-to control symptoms (Cogentin,
Artane, Symmetrel); anticholinergics drugs act • An autoimmune disorder, characterized by varying
at central sites to inhibit cerebral motor
degrees of weakness of the voluntary muscles
impulses that cause rigidity of themusculature
(Smeltzer & Bare, 2004, p. 1956)
• MAOI-Bomcriptine; inhibit breakdown of
dopamine • Highest in young adult females.

• Physiotherapy-reduces rigidity of muscles and


prevents contractures Manifestations
Subjective:
• Surgical intervention-to destroy globus pallidus  Extreme muscle weakness, worsens as the
(to relieve rigidity) and/or thalamus (relieve muscle is used but disappears with rest
tremors)
 Dysphagia

Nursing Management  Diplopia (double vision)


• Provide safe environment
 Dysarthria
• Nutrition
Objective:
 Ptosis of the eyelid (both eyes)
 Small bite pieces of food to prevent
choking  Myasthenia smile (nasal smile)
 Small frequent meals for easy
 Strabismus
mastication
Note:
 Adequate intake of roughage to prevent Myasthenia gravis is purely a motor disorder with NO
constipation effect on sensation or coordination (Smeltzer & Bare, 2004, p.
1956)
 Encourage diet rich in nutrient-dense
foods such as fruits, vegetables, whole
Diagnostic Test
grains
 Neostigmine (Prostigmine)—subcutaneous or IV
administration of tensilon (prevents enzymatic
• Positioning and activity
breakdown of Ach) to provided relief of symptoms

 Limit postural activities  The thymus gland, which is a site of acetylcholine


receptor antibody production is enlarged in
 Maintain gait as normal as possible: myasthenia gravis (Smeltzer & Bare, 2004)
may utilize cane or wheel chair

 Encourage daily physical therapy to Medical Management


limit rigidity and prevent contractions  Pharmacologic

 Medication compliance; report side - Acetylcholinesterase blockers


effects
- Corticosteroids to suppress immunity
• Avoid rushing client as he is unable to work
under pressure  Plasmapheresis -

• Assist client in setting achievable goals to  X-ray or surgical removal of thymus (thymectomy)
improve self-esteem

• Total body function support in advanced stages


(respiratory elimination)
Myasthenic Crisis
• Sudden inability to swallow or maintain respirations
due to weakness of the muscles of respiration;
undermedication

• Exacerbation of the disease process characterized by


severe generalized muscle weakness and respiratory
and bulbar weakness that may result in respiratory
Myasthenia Gravis failure (Smeltzer & Bare, 2004, p.1957)
• Disturbance in the transmission of impulses at the
myoneural junction resulting in profound weakness Cholinergic Crisis
(muscle of the eyes, eyelid, chewing, swallowing, • Overdose of anticholinergic drugs
speaking and breathing)
• May mimic the symptoms of exacerbation 3. Prevent complications

Note: 4. Emotional support


Differentiation of myasthenic crisis and
cholinergic crisis can be achieved with the edrophonium
chloride (Tensilon) Test. The patient with myasthenic
crisis improves immediately following administration, while Client with Multiple
patient with cholinergic crisis may experience no
improvement or deteriorate (Smeltzer & Bare, 2004) Sclerosis
1. Believed to be autoimmune response to prior viral
infection

Guillain-Barre Syndrome 2. Inflammation destroys myelin leading to axon


dysfunction; neurons in spinal cord, brain stem,
• Immunologic status often follows respiratory or GIT
cerebrum, cerebellum and optic nerve affected
infection, viral immunization, trauma or surgery
3. Stressors trigger multiple sclerosis—febrile states,
• An autoimmune attack of the peripheral nerve
pregnancy, physical exertion and fatigue and these
myelin (Smeltzer & Bare, 2004). can trigger relapses
• Areas of demyelination in the motor cells of the 4. Incidence is highest in young adults (20-40); onset
spinal cord and medulla (ascending loss) vs. ALS between 20-50; females more than males
(descending)

• Seen in adults 20-50 years


Manifestations
1. Fatigue
• After initial and plateau periods recovery in 1 year
sometimes with residual deficits, other dies of
complications 2. Optic nerve involvement: blurred vision, haziness

3. Brain stem involvement: nystagmus, dysarthria


ALS- common in males (scanning speech); cognitive dysfunction, vertigo,
deafness
Manifestations
- begins with muscle weakness and 4. Weakness, numbness in legs, spastic paresis,
diminished reflexes of the lower bladder and bowel dysfunction
extremities
5. Cerebellar involvement: nystagmus , ataxia,
hypotonia
Subjective:
6. Blindness
 Generalized weakness

 Paresthesia

 Diplopia
Meningitis
• Inflammation of pia matter, arachnoid and
Objective subarachnoid space
 Ascending paralysis within the body usually
24-72 hours • Spreads rapidly through CNS because of circulation
of CSF around brain and spinal cord
 Respiratory paralysis
• May be bacterial, viral, fungal, parasitic in origin
 Hypertension, tachycardia and low grade
fever • Infection enters CNS though invasive procedure or
through bloodstream, secondary to another infection
 Incontinence in body

Medical Management Bacterial Meningitis


1. Steroids
• Causative organism: Neisseria meningitides,
2. Plasmapheresis Streptococcus pneumonia, Haemophilus influenza,
Escherichia coli
3. Support of vital function
• Manifestations

Nursing Management: Supportive care a. Fever, chills


1. Respiratory management
b. Headache, back and abdominal pain
2. Nutritional management
c. Nausea and vomiting
d. Meningeal irritation: 4. Manifestations depend on rate of onset: progressive
cognitive dysfunction, gait disruptions, urinary
 Nuchal rigidity (stiff neck)-early sign incontinence

 Positive Kernig’s sign • Visual changes

 Positive Brudzinski’s sign-when the patient’s • Increase in head size


neck is flexed, flexion of the knees and hips
is produced • Increase ICP

 Photophobia –extreme sensitivity to light


Treatment/Management
e. Meningococcal meningitis: rapidly spreading 1. Diuretics
petechial rash of skin and mucous membrane
2. Surgery
f. Increased ICP: decreased LOC, papilledema –
edema of optic disc due to increased ICP 3. Protect from injury from altered LOC and immobility

Viral Meningitis
• Less severe, benign course with short duration,
intense headache with malaise, nausea, vomiting,
Skeletal muscle
lethargy, signs of meningeal irritation
• Attach to the skeleton
Encephalitis • Permits voluntary movements
1. Acute inflammation of parenchyma of brain or spinal
cord
• Maintain posture
2. Usually caused by virus
• Generates heat

• Innervated by the somatic nervous system


Medications
1. Meningitis: immediate treatment of effective
• Produce movement by contraction
antibodies for 7-21 days according to culture
results; dexamethasone to suppress inflammation
• Sarcomeres-functional unit of striated muscle
Dilantin—Increase seizure threshold

Health Promotion Basic Principles of skeletal muscle action


1. Vaccinations for meningococcal, pneumococcal, 1. Motor unit should be stimulated to contract, absence
haemophilus meningitis of impulse conduction leads to paralysis

2. Prophylactic rifampins for persons exposed to 2. Muscles are attached to at least 2 bones; with each
meningococcal meningitis contraction, muscle’s insertion bone moves and the
muscle origin bone remains stationary
3. Mosquito control
3. Bone serve as levers; joint as fulcrums
4. Prompt diagnosis

5. Asepsis care for clients with open head injury or


neurosurgery
Fractures
- Break in the continuity of bone

Classification:
Hydrocephalus  Closed-no break in the skin
• Increase in volume of CSF within ventricular system,
which becomes dilated  Open-

Common Cause:  Complete-involves break across the entire


1. Noncommunicating obstruction in CSF drainage from cross-section of the bone and is frequently
ventricular system displaced

2. Communicating: CSF is not effectively reabsorbed  Incomplete e.g. greenstick, the break
through arachnoid villi occurs through only part of the cross-
section of the bone
3. Normal pressure hydrocephalus: occurs in
persons>60 in which ventricles enlarge causing  Displaced
cerebral tissue compression
 Comminuted-several bone fragments

 Impacted or compression
 Complicated-accompanied by infection
Purposes:
 Pathologic-systemic, loss of bone density 1. Immobilization

2. Prevention or correction of deformity


Clinical Manifestations
• Deformity 3. Maintenance support and protection to realign bone

• Swelling 4. Promotion of healing which allows early weight


bearing
• Bruising

Nursing Management: CAST


• Muscle spasm
Precast application
• Tenderness
- Care- factual and sensory information
• Pain
- Contraindications

• Impaired sensation Intracasting


Postcasting
• Loss of normal function - Drying 24-48 hours

• Crepitus- grating sensation resulting from - Proper handling


rubbing of bone fragments against each other
- Watch for neurovascular complications
• Abnormal mobility of affected part
- Watch for infection
• Hypovolemic shock
- Watch for cast syndrome (occurs with body
casts)
Vasogenic shock-due to severe pain
 Prolonged nausea and vomiting

 Abdominal distention and pain


Surgical/Medical Management
 Open-reduction-alignment during surgery
Cast syndrome-psychological (claustrophobic
reaction) and physiologic (superior mesenteric artery
 Internal fixation device placement: use of
syndrome) responses to confinement in body cast
screws, wires, nails or rods
(Smeltzer & Bare, 2004)
 Closed reduction
- Watch for: wet-spots-drainage: hot spots-
tissue infection or necrosis under casts
 Traction application
- Elevated injured extremity especially for the
 Management of shock first 24-48 hours

- Prevents disuse syndrome


Nursing Management for Fractures • Exercise joints before and after
injured site
1. Assess neurovascular status (6 P’s)
• Isometric exercises, gluteal setting,
abdominal tightening and deep
ulselessness
breathing exercises
allor
ain
• Skin care
aresthesia
oikilothermia
aresia/paralysis • Elimination

2. Assess skin • Nutrition- Vit C (absorption of


calcium)
3. Assess for fat embolism-long bone fracture, may
occur 24-48 hours after injury

4. Analgesics-Opioid analgesics
Cast care
5. Rehabilitation  Keep cast dry; use plastic when bathing

 Do not use powder or insert objects inside cast

Cast Application
 Use of slings/crutches to enhance comfort safety and Principles of Effective Traction
ambulation  Traction must be continuous to be effective in
reducing and immobilizing fractures
 Reportable conditions:

- Increased swelling
 Skeletal traction is never interrupted

 Weights are not removed unless intermittent traction


- Tingling or burning sensation
is prescribed
- Inability to move muscle around cast
 Any factor that might reduce the effective pull or
alter its resultant line of pull must be eliminated:
- Foul odor inside or around the edge
- Patient must be in good body alignment in the
center of the bed when traction is applied
Therapeutic Traction
- Pulling force - Ropes must be unobstructed

- Weights must hang free and not rest on the


Types: bed or floor
1. Skin
- Knots in the rope or the footplate must not
2. Skeletal touch the pulley or the foot of the bed

3. Cervical - (Smeltzer & Bare, 2004, p. 2026)

4. Pelvic
Nursing Care of Clients with Braces or
5. Buck’s traction (unilateral or bilateral) is skin Splints
traction to the lower leg
1. Check body and equipment alignment
6. Russel’s – one leg is higher than the other
2. Keep equipment in good condition

3. Examine integumentary integrity


Techniques:
1. Running (Straight) applies the pulling force in a
straight line with body part resting on bed

2. Suspension (Balanced)-supports the affected


extremity off the bed and allows for some patient Use of Cane
movement without disruption of the line of pull 1. Ascertain client capability to bear weight

3. Continuous intermittent 2. Ensure strength of upper extremity opposite lower

Care of Client
1. Know the purpose and contraindicated movements

2. Pin site care-goal is avoid infection and development


of osteomyelitis; site is covered with a sterile
dressing (Smeltzer & Bare, 2004, p. 2028)

3. Ropes and pulley should hang free

4. Monitor color, warmth, movement and sensation of


extremity distal to the traction every 4-8 hours
( neurovascular check)

5. Devices such as trapeze, fracture pins

6. Immobility problems (thrombophlebitis, diversional extremity


therapies , among others)
3. Ensure proper length of cane

After traction:  Highest point approximately at level of


 Gradually assume sitting position greater trochanter

 Lack of proprioception response initially  30 degrees flexion of elbow

 Joints may be unstable; may feel faint or weak  Tip of the cane 15 cm (6 inches) lateral to
for a while the base of the fifth toe (Smeltzer & Bare,
2004, p. 174)
4. Ensure proper techniques  Disease involving degeneration and or
inflammation of joints and surrounding
 Opposite affected extremity structures

 Affected extremity cane simultaneously  Out of 100 types of with unknown cause

 Should be close to the body  Common types:

5. Observe for incorrect use 1. Inflammatory –RA and SLE

 Leaning the body over the cane 2. Non-inflammatory –degenerative joint


disease
 Shortening the stride of the unaffected side
3. Gout-crystal-produce disease from high
 Persistence of abnormal gait protein ingestion

Crutch Osteoarthritis
Nursing care  Autosomal recessive trait causing cartilages to
1. Ensure readiness of client wear out or repair less effective; localized; NO
synovial membrane swelling
 Strength of upper torso
o Wear and tear of joints
 Psychological fitness
o Obesity; joint trauma
2. Ensure proper fit
o Aging: 55 years old and above
 Axillary bars 5 cm (2 inches below axilla),
15 cm (6 inches infront and lateral) tripod o Degeneration and atrophy of the
position cartilage and calcification of ligaments

3. Assist in use of proper technique o Primarily affects weight-bearing joints,


spine and hands
 Four point- R crutch, L foot, LC, RF
 Degeneration of cartilages into the bony spur
 Two-point-R crutch with L foot, then LC with
RF  Formation of subchondral osteophyte

 Three point-advance both crutches and  Secondary synovitis (late manifestation)-pain


weak extremity, then follow good foot and swelling with joint movement

 Swing to gait-advance crutches then swing


feet to the level of the crutches

 Swing through gait-advance crutches then Manifestations:


swing through the crutches  Joint stiffness

4. Incorrect position  Pain after exercise; pain with movement

 Walking on ball of foot  Heberden’s (distal) and Bouchard’s (proximal)


nodes
 Hunching shoulders
 Decreased ROM
 Looking downward
 Crepitus
 Hiking hips (common in amputees)
Medical Management
 Bearing weight under arms may cause  Steroids
brachial plexus damage
 Antiinflammatory
 Lifting crutches while still bearing down on
them  Analgesics-salicylates and NSAIDs

5. Evaluate client’s response  Physiotherapy/Exercise

 Surgery-replacement of mobility (knee and hips


common)

Arthritis
Rheumatoid Arthritis
 Systemic with synovial membrane inflammation bone slips over another and eliminates the joint space
with blood, fibrin, and coagulation deposits (Smeltzer & Bare, 2004, p. 1621)

 Unknown cause: hereditary, autoimmune Gouty Arthritis


psychophysiologic factors, 25-55 years old  Mono-articular (one joint)

 Exacerbations linked to physical and emotional  Hyperuricemia; 40-50 years old


stress
1. Genetic increase in purine
 Inflammatory changes in the connective tissue metabolism and production

2. Ingestion of excessive alcohol or high


Pathophysiology: purine diet
Symmetrical joints

Synovial lining of joints become inflamed


Pathophysiology:
Synovitis
Uric acid-major by product of protein and nucleic acid
Increased fluid with pannus metabolism
Pannus destroys cartilage and invade joint capsule Tendency to crystallize especially with dehydration, diuretics
use and increased
Replaced by fibrous connective tissues
Tubular resorption to the systemic circulation
Affects tendons and ligaments
Deposited in connective tissues and joints (esp. great toe)
Cause joint subluxation, bony ankylosis and
consolidation of joints Release of lysosomal enzymes
Swelling, deformities Inflammation
Pain Joint degeneration and disability and tophaceous (white in
Manifestations: color) deposits in the joints
Subjective
 Fatigue, malaise, anorexia May cause renal tubular damage leading to renal stones and
failure
 Joint pain, stiffness after periods of
inactivity especially a.m
Note:
 Paresthesia (destruction of nerve Attacks of gout appear to be related to sudden
involved) increases or decreases of serum uric acid levels. When
the urate crystals precipitate within a joint, an
Objective inflammatory response occurs and an attack of gout
 Joint inflammation and deformity begins. With repeated attacks, accumulation of sodium
urate crystals, called tophi, are deposited in peripheral
 Swan neck and Boutinniere areas of the body, such as great toe, the hands, and the
deformities; ulnar drift, joint ear (Smeltzer & Bare, 2004, p. 1630).
subluxation
Manifestations:
- Tight/reddened skin around inflamed joint,
 Increased ESR, low grade fever ,
edema
positive rheumatoid factor
- Pain
 Anemia, weight loss
- Increase temperature
Medical Management
- Hyperuricemia> 7.5 mg/dl
 Coticosteroids, anti-inflammatory,
analgesics, immune suppressive drugs
Management of Gout
1. Decrease protein in diet
 Plasmapheresis
2. Weight control and decrease alcohol ingestion
 Antimalarial drugs—destroys
autoimmune antibodies
3. Increase fluids to 3000 ml/day (the more
dehydration, more crystallization)
 Cytotoxic drugs
4. Joint rest
Note:
Deformities of the hands and feet are common
5. Allupurinol/Probenecid, Colechicine
in RA. The deformity may be caused by misalignment
resulting from swelling, progressive joint destruction, or
the subluxation (partial dislocation) that occurs when
High Purine foods
1. Poultry

2. Organ meats

3. Meat extracts

4. Seafoods, sardines, anchovies, shrimp herring

5. Asparagus, spinach, mushroom

Surgical intervention
1. Arthrodesis-surgical fusion of a joint to render a joint
immobile but decreases pain and increases strength

2. Osteotomy-transection of a bone to correct a


deformity or misalignment

3. Resection-for partial removal of a degenerated bone


(wrist and foot)

4. Replacement arthroplasty-joint replacement

Assistive devices:
1. Eating utensils

2. Braces

3. Walkers

4. Cane-single, quad

Therapies
1. Diversion

2. Exercise, ROM, quadriceps exercise

3. TENS

4. Cold and warm pack 30 minutes before activities

5. Whirl pool bath

6. Balance rest and activity

7. Assistive devices, elevated chair or toilet to 3-4


inches

Nursing Diagnosis
• Chronic pain related to joint degeneration

• Impaired physical activity r/t restricted


mobilization

• Activity intolerance

• Self-care deficit

• Body image disturbance r/t visible body


changes/deformities/misalignment

• Knowledge deficit

• Sleep pattern disturbance

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