Lecturer: Mr. Jake D.

Diputado BSN, RN

DISTURBANCES IN PERCEPTION AND COORDINATION

PERCEPTION Conscious recognition and interpretation (awareness) of the sensory stimuli that serve as a basis for understanding, learning, and knowing or for the motivation of a particular action or reaction

COORDINATION When action or reaction towards a stimulus is occurring in a PURPOSEFUL, ORDERLY FASHION; appropriate response to a stimulus

ROLES OF THE NERVOUS SYSTEM

Reciprocally

interact with the

environment Maintain homeostasis (with the endocrine system)

FUNCTIONS
Sensory: interpret incoming stimulus/information Integrative: analyze, store, make decisions regarding appropriate behavior Motor: initiating muscular or glandular activity; ongoing and evolving interaction with the environment

VENTRICLES AND CSF

Ventricles: four fluid-filled cavities within the brain that connect to one another with the spinal cord CSF: formed in the choroid plexus; about 135 cc; cushions, provides nutrients, allow fluid shifts

3 ESSENTIAL COMPONENTS OF THE SKULL

Brain tissue = 78% Blood = 12% CSF = 10% Monro-Kellie Hypothesis: if the volume added to the cranial vault equals the volume displaced from it, the total intracranial pressure will not change; ICP is therefore constant Normal ICP = 60-150 cmH2O or 0-15 mmHg

NORMAL COMPENSATORY ADAPTATIONS

Initial

Increased CSF absorption Displacement of CSF into the subarachnoid space Collapse of the cerebral veins and dural sinuses
Distensibility of the dura Increased venous outflow Decreased CSF production Constriction and vasodilation Slight compression of brain tissue

Other mechanisms

CEREBRAL BLOOD FLOW

Amount of blood in milliliters passing through 100 grams of brain tissue in one minute Global CBF = approximately 50 ml/min Brain needs constant supply of O2 and glucose (20% of the bodys O2 and 25% of the bodys glucose)

SOURCES OF BLOOD SUPPLY

Internal carotid arteries: anterior circulation; ipsilateral hemispheres Vertebral arteries: posterior circulation, posterior fossa Circle of Willis: acts as safety valve; arises from basillar arteries and internal carotid arteries Cerebral arteries: anterior, middle, posterior (2 each) Jugular veins: drains the brain venous blood through dural sinuses

SPECIAL CHARACTERISTICS OF CEREBRAL PERFUSION

1) Autoregulation

3 physiologic mechanisms
Changes

in ICP Cerebral vasodilation Metabolic factors

Mean Arterial Pressure (MAP): pressure at which autoregulation is effective (70-105 mmHg) Upper limit is 150 mmH MAP = SBP+2 (DBP) 3

AUTOREGULATION CONTD.

Cerebral Perfusion Pressure: needed to ensure blood flow to the brain

CPP

= MAP ICP As CPP decreases, autoregulation fails and CBF diminishes

30

mmHg is incompatible with life

2) Blood-Brain Barrier: physiologic barrier between blood capillaries and brain tissue

NEUROPHYSIOLOGY
Neurotransmission: conduction of an impulse throughout the nervous system Neurons: receive and transmit impulses; nonmitotic; excitable, conductive and can influence other cells

TRANSMISSION WITHIN THE NERVE FIBERS

Action Potential
Chemical

gradient Electrical gradient

Propagation of Action Potential

Resting

stage: (+) outside, (-) inside Depolarization phase: (-) outside, (+) inside

TRANSMISSION ACROSS SYNAPSES

Chemical/electrical Neurotransmitters

Acetylcholine Biogenic amines

Dopamine Norepinephrine Serotonin Histamine

Amino acids
GABA Peptides

TYPES OF NEURONS

Neuroglia: protect and nourish neurons; mitotic

Type Astrocytes Microglia Oligodendrocytes Ependymal cells Schwann cells Functions Supply nutrients Provide protection against microorganisms Wrap tightly around nerve fibers to form myelin sheath Ciliated; line brain cavities; form CSF Phagocytic cells that form myelin sheath around nerve fibers Found in the PNS; maintain chemical balance of neurons

Satellite cells

Cranium and cerebral: composed of 8 cranial and facial bones Foramen magnum: largest hole through which the brain stem extends to the spinal cord Vertebral column: protects the spinal cord, supports the head, and provides flexibility; strengthened by ligaments and intervertebral discs

CENTRAL NERVOUS SYSTEM

Cerebrum: 2 hemispheres joined by Corpus Callosum; cerebral cortex (outer surface of the cerebrum); basal ganglia is located deep within Diencephalon: embedded in the brain superior to the brain stem

Thalamus:

process sensory impulses before it reaches cerebral cortex Hypothalamus: regulates endocrine and autonomic functions

THE BRAIN

CNS CONTD.

Brainstem
Midbrain: auditory and visual reflexes Pons: contains the fiber tracts and nuclei that control respirations

Medulla: control cardiac rate, BP, respirations, and swallowing Reticular Activating System (RAS): influence excitatory and inhibitory control of motor neurons; regulatory system for consciousness

CNS CONTD.
Cerebellum: 2 hemispheres; coordinaton of skeletal muscle activity; maintenance of balance, posture, and control of the voluntary movements Spinal cord: extends from the medulla up to the first lumbar vertebra; gives rise to 31 pairs of spinal nerves (C1-C7, T1-T12, L1-L5, S1-S5, coccygeal nerve); reflex center

TRACTS IN THE SPINAL CORD

Ascending: carry sensory information to higher levels of CNS

Spinocerebellar tracts: muscle tension and body position Spinothalamic: pain and temperature sensation Pyramidal tracts: cortex to cranial and peripheral nerves; inhibits muscle tone Extrapyramidal: brain stem, basal ganglia, and cerebellum; maintains muscle tone and gross body movements Upper motor neurons: from cerebral cortex to anterior gray column of spinal cord; spasticity and hyperactive reflexes Lower motor neurons: final common pathways; from anterior gray column up to muscles; flaccidity and loss of reflexes

Descending (Corticospinal)

REFLEX ARC
Spinal cord mediates most reflexes automatic/perceptible, inhibited, or conditioned

Hyperreflexia:

disease or injury of certain descending motor tracts Hyporeflexia: damage or degeneration of the sensory/motor nerves

REFLEX
is an involuntary and nearly instantaneous movement in response to a stimulus reflex actions are mediated via the reflex arc For a reflex, reaction time or latency is the time from the onset of a stimulus until the organism responds. In animals, reaction time to visual stimuli is typically 150 to 300 milliseconds.

STRETCH REFLEXES
(often called deep tendon reflexes) provide information on the integrity of the central nervous system and peripheral nervous system. Generally, decreased reflexes indicate a peripheral problem, and lively or exaggerated reflexes a central one.

EXAMPLES OF STRETCH REFLEXES

Biceps reflex (C5, C6) Brachioradialis reflex (C5, C6, C7) Extensor digitorum reflex (C6, C7) Triceps reflex (C6, C7, C8) Patellar reflex or knee-jerk reflex L2, L3, L4) Ankle jerk reflex (Achilles reflex) (S1, S2) Plantar reflex or Babinski reflex (L5, S1, S2)

REFLEXES INVOLVING THE CRANIAL NERVES

Name Sensory Motor III III V VII III, IV, VI + X Pupillary light reflex II Accommodation reflex Jaw jerk reflex Corneal reflex, also known as the blink reflex Vestibulo-ocular reflex Gag reflex II V V VIII IX

GRADING REFLEXES
Grade 0 1+ or + 2+ or ++ 3+ or +++ 4+ or ++++ Description Absent Hypoactive "Normal" Hyperactive without clonus Hyperactive with clonus

NORMAL REFLEXES

ABNORMAL REFLEXES

PERIPHERAL NERVOUS SYSTEM

Cranial Nerves: innervate head and neck region, except the vagus nerve; all come out of the brain stem Spinal nerves

Plexuses:

complex cluster of nerve fibers (cervical, brachial, lumbar, sacral region) Dermatomes: area of the skin innervated by cutaneous branches of a single spinal nerve

SOMATIC NERVOUS SYSTEM

Motor and sensory nerves Controls skeletal muscles Produces a motor response through efferent nerve fibers from CNS which transmit impulses to the skin and skeletal muscles

AUTONOMIC NERVOUS SYSTEM

Controls invountary or automatic body functions; has two subdivisions, serving same organs but have counterbalancing effects; each system can inhibit the organ stimulated by the other Sympathetic System: functions mainly during stress (fight-or-flight response); open all except GI and GU Parasympathetic System: supports restorative, resting body functions; close all except GI and GU

Effector Organ 1) Heart 2) Lungs 3) GIT motility and tone sphincters 4) Urinary bladder Muscle and sphincter 5) Liver

Sympathetic Increased rate and contractility Relaxation Contraction Relaxation Contraction Glycogenolysis

Parasympathetic Decreased rate and contractility Contraction Relaxation Contraction relaxation none

THE SPECIAL SENSES

SENSE OF SIGHT
Normally

form a clear retinal image of an object at 20 feet away (20/20 vision) Binocular vision: ability to judge relative distances of objects

ANATOMY OF THE EYEBALL

Outer

Cornea: thin, tough, transparent layer supplied with sensory nerves; no blood supply; O2 and glucose through diffusion Sclera Choroid: highly vascular; dark-brown membrane Ciliary body: contract and dilate ciliary process which contain capillaries that secrete fluid Iris: visible colored part of eye; control pupil size Retina: neural tissue; phagocyte; stores vitamin A; contains rods and cones Fovea centralis: responsible for colored vision

Middle

Inner

Small eyeball: farsightedness Big eyeball: nearsightedness

PHYSIOLOGY OF VISION
Formation of an image on the retina accomplished by the following: Refraction Accomodation Constriction of pupils Convergence of the eyeballs

STIMULATION OF THE RETINA

Dim light: breakdown of rhodopsin in rods Cones: responsible for daylight and color vision; detects red, green, and blue Fovea centralis: where cones are concentrated Conduction to central area in the occipital lobe

SENSE OF HEARING

Parts:
Outer:

collects sound Inner: conducts sound

Tympanic

membrane or ear drum: normally pearly gray in color

INTERPRETATION OF SOUND

Loudness: intensity; stimulates organ of Corti

Decibels:
Normal

unit of measure of intensity of sound

conversation: 65 dB Amplified rock music: 120 dB Nearby jetplanes: 140 dB Above 85 dB: can damage organ of Corti

Pitch: frequency; normal person can hear 162000 Hz; speech falls in the range of 85-1050 Hz

Cerebrovascular Accident

STROKE

STROKE/BRAIN ATTACK

Needing emergency management; no allowances for worsening are tolerated; treatable and preventable

TYPES OF STROKE

Ischemic Stroke Thrombotic: formation of a blood clot or coagulation that results in the narrowing of the lumen of a blood vessel with eventual occlusion Embolic: occlusion of a cerebral artery by the embolus, resulting in necrosis and edema of the area supplied by the involved vessel Hemorrhagic Stroke Intracerebral hemorrhagic stroke: bleeding within the brain caused by a rupture of the vessels Subarachnoid Hemorrhagic Stroke: caused by aneurysm

DEVELOPMENT OF CVA

TIA: brief episodes of neurologic manifestations which clear completely in 24 hours Reversible Ischemic Neurologic Deficit: neurologic deficit remain after 24 hours but leaves not residual signs and symptoms after days to weeks Stroke-in-Evolution: progressing; develops over a period of hours or days; manifestations dont resolve and leave residual neurologic effects Complete stroke: neurologic deficits remain unchanged within 2-3 days period

RISK FACTORS FOR STROKE

Prior ischemic episodes Cardiac disease Diabetes Mellitus Atherosclerotic disease Hypertension; hypercholesterolemia Polycythemia Smoking Oral contraceptives Emotional stress Obesity Family history of stroke Age

WARNING SIGNS THAT MAY PRECEDE CVA

Paresthesia Transient loss of speech Hemiplegia Occipital/nuchal headache Vertigo Syncope Motor-sensory disturbances (tingling, transient paralysis) Epistaxis

SPECIFIC DEFICITS (DEPENDENT UPON AREA DAMAGED)

Hemiplegia Aphasia Sensory/receptive Motor expressive Global/receptive-expressive Agnosia Dysarthria Incontinence Horners Syndrome: sunken eyeballs; less/no lacrimation Unilateral neglect

EMOTIONAL/BEHAVIORAL REACTIONS
Severe mood swings Social withdrawal Inappropriate sexual behavior Frustration/angry outbursts Regression

RIGHT Brain Hemisphere Damage

Paralyzed left side Spatial-perceptual deficits Tends to deny or minimize problems Impaired judgment Impaired time concepts Short attention span

LEFT Brain Hemisphere Damage

Paralyzed right side Impaired speech and language Impaired right/left discrimination Aware of deficits; depression/anxiety Impaired comprehension Slow performance Cautious

MIDDLE CEREBRAL ARTERY INVOLVEMENT

Contralateral paralysis Contralateral anesthesia, loss of proprioception, fine touch, localization Aphasia Neglect of opposite side Homonymous hemianopia

DIAGNOSTIC PROCEDURES
CT Scan MRI Angiography CBC, PT, PTT: not definitive to confirm diagnosis

MEDICAL MANAGEMENT
Decrease ICP: osmotic diuretics BP Management: antihypertensives Fluid volume management: diuretics Antithrombotic (aspirin, dipyridamole) Anticoagulant (heparin, clexane) Tissue plasminogen activator: dissolves clot and must be given within 3 hours of onset of manifestations; recombinant altephase

NURSING MANAGEMENT

Hourly neurologic assessment Monitor and prevent intracranial hypertension Positioning/Activity Bed rest: unaffected side Pillows for support to prevent flexion deformity, thrombus formation, and external hip rotation Progressive activity and ADL Prevent injury: normal saline/artificial tears to eyes; eye patch; side rails up; prevent decubitus ulcer; oral care

NURSING MANAGEMENT CONTD.

Nutrition: prevent aspiration Communication; reorientation; reduce environmental stimuli; emotional support

DISCHARGE CARE

Ways to prevent recurrence

Dietary

modification Stress reduction Exercise program Drug compliance

Residual deficits and balancing realistic expectations Special methods of feeding Ensure continuity of care and emotional support

SPINAL CORD INJURIES

SCI
Damage to C4 can already cause death; C4 is the major innervation to the disphragm Usually due to trauma Most common in 16-30 y.o. Causes: MVA, falls, violence, sports injuries Physical description:

Concussion,

contusion, laceration, transection, hemorrhage, damage to blood vessels supplying spinal cord Fractured vertebrae damage cord

PATHOPHYSIOLOGY
Primary injury causes microscopic hemorrhages in gray matter of cord and edema of white matter of cord Microcirculation of cord impaired by edema and hemorrhage; further impaired by vasospasm Necrosis of gray and white matter occurs and function of nerves through impaired area is lost

PATHOPHYSIOLOGY CONTD.

Acceleration and deceleration injuries result in abnormal spinal cord movements

Hyperflexion:

forcible forward bending Hyperextension: forcible backward bending Axial loading: form of compression applying vertebral force Excessive rotation: causing compression fractures Other causes: penetration by bullets or foreign objects

CLASSIFICATIONS

Complete SCI
total

loss of motor and sensory function below level of injury loss of function below level of injury

Incomplete SCI
variable

MANIFESTATIONS
Subjective: loss of sensation below injury level; inability to move Objective:

Early

symptoms of spinal shock:

of reflexes and flaccid paralysis below level of

Absence

injury Hypotonia results in bowel and bladder distension Inability to perspire in affected parts hypotension; bradycardia

MANIFESTATIONS CONTD.

Objective contd.:
Later

Symptoms

Reflex

hyperexcitability Decreased reflex hyperexcitability below site in all instances of cord damage following hyperreflexia In total cord damage : loss of motor and sensory function is permanent
Sacral: atonic bladder and bowel with impairment of sphincter control Lumbar: spastic bladder; loss of bladder and bowel control Thoracic: trunk below diaphragm Cervical: from neck down; if above C4 respiration is depressed

SCI CONTD.
C1-C4: Death C5-T3: Quadriplegia T4-S4: Paraplegia Back Pain: Disc Herniation and/or Spinal Stenosis

AUTONOMIC DYSREFLEXIA

Exaggerated autonomic response to a stimulus, such as:

Distended

bladder/bowel Pain sensation Severe hypertension Headache Flushed skin Diaphoresis Nasal congestion

AUTONOMIC DYSREFLEXIA CONTD.

Management
High

Fowlers position Ensure patency of urine drainage and assess for impaction Analgesic for pain Antihypertensive as prescribed

NURSING DIAGNOSES: SCI

Impaired Gas Exchange (paralysis) Decreased Cardiac Output R/T Venous Pooling and Immobility Impaired Skin Integrity Constipation Urinary Retention Impaired Physical Mobility Risk for Autonomic Dysreflexia Altered Nutrition: Less than Body Requirements Sexual Dysfunction Risk for Injury Altered Family Processes Risk for Ineffective Individual Coping Body Image Disturbance

MEDICAL MANAGEMENT

Immobilization: Gardner-Wells tongs; Halo external fixation Atropine: maintenance of heart rate Dopamine: increase BP Methylprednisolone Therapy: reduce edema and inflammation NGT Intubation Indwelling urinary catheter Stress ulcer prophylaxis (H2 blockers; PP inhibitors) Physical therapy

GARDNER WELLS TONGS

SPINAL SHOCK
Also known as neurogenic shock; sudden depression of reflex activity in the spinal cord that occurs below the level of injury (areflexia) Occurs within the first hour of injury and can last days to months Muscles become completely paralyzed and flaccid, and reflexes are absent. Ends when the reflexes are regained

ASSESSMENT
Flaccid paralysis Hypotension Bradycardia Loss of reflex activity below the level of injury Paralytic ileus

INTERVENTIONS
Monitor for signs of spinal shock following a spinal cord injury. Monitor for hypotension and bradycardia. Monitor for reflex activity. Assess bowel sounds. Monitor for bowel and urinary retention. Provide supportive measures as prescribed, based on the presence of symptoms Monitor for the return of reflexes.

AUTONOMIC DYSREFLEXIA
Also known as autonomic hyperreflexia Commonly caused by visceral distention from a distended bladder or impacted rectum A neurologic emergency; must be treated immediately to prevent hypertensive stroke Generally occurs after the period of spinal shock is resolved Occurs with lesions or injuries above T6 and in cervical lesions

ASSESSMENT

HPN Bradycardia Flushing of the face and neck Severe, throbbing headache Nasal stuffiness Piloerection (goose flesh) Sweating Nausea Restlessness Dilated pupils & blurred vision

INTERVENTIONS

Immediate interventions:
a) b) c)

d)

e) f)

Elevate the head of bed Loosen any tight clothing Remove the cause: check for bowel or bladder distention; if with Foley cath, check if there are kinks in the tubing Check for fecal impaction; disimpact the client if necessary Notify physician Administer anti-HPN as prescribed

CERVICAL TRACTIONS
Or skeletal traction; are used to stabilize fractures or dislocations of the cervical or upper thoracic spine Types: skull (cervical) tongs (ex. Gardner-Wells tongs) & halo traction (halo fixation device)

SKULL TONGS
Are inserted into the outer aspect of the skull, & traction is applied Weights are attached to the tongs, and the client is used as countertraction. Monitor neurologic status of client. Determine the amount of weight prescribed to be added to the traction. Ensure that weights hang securely and freely at all times.

SKULL TONGS
Ensure that the ropes for the traction remain within the pulley. Maintain body alignment and maintain care of the client on a special bed (ex. Roto-Rest bed, Stryker, or Foster frame) as prescribed. Turn the client every 2 hours. Assess insertion site of the tongs for infection. Provide sterile pin site care as prescribed.

HALO TRACTION
A static traction device that consists of a headpiece with four pins, two anterior and two posterior, inserted into the clients skull The metal halo ring may be attached to a vest (jacket) or cast when the spine is stable, allowing increased client mobility.

Monitor neurologic status. Never mover or turn the client by holding or pulling on the traction device Assess for tightness of the jacket or cast is not causing pressure. Provide sterile pin site care as prescribed.

BRAIN TUMORS

BRAIN TUMORS
Primary: tumors arising from the brain or its supporting structures Secondary: those metastasizing from other areas in the body

BRAIN TUMORS CONTD.

Most primary brain tumors do not metastasize out of the brain to other areas Etiology unknown, but familial tendencies, immunosuppression, and environmental factors are being considered.

PATHOPHYSIOLOGY

Space-occupying lesions
Tumor

displaces normal tissue or occupies normal tissue spaces Brain tissue compressed, blood flow altered, ischemia, necrosis

Increased ICP
Cerebral

edema; Displacement of brain structures may lead to brain herniation

PATHOPHYSIOLOGY CONTD.

Intracranial Tumors May be encapsulated, nonencapsulated, or invasive Glial tumors/Gliomas: tumors of the neuroglia (supporting brain tissue); astrocytomas are the most common type Oligodendrogliomas: tumors of the white matter of the brain Ependymomas: 4th ventricle and within the SC tissue Pituitary tumors: mostly benign, small, encapsulated Meningiomas: mostly benign; may involve all meningeal layers Acoustic Neuromas: tumors of the Schwann cells of the 8th cranial nerve, the acoustic nerve/or vestibulocochlear

CLINICAL MANIFESTATIONS
Mental status changes: decreased LOC, confusion, disorientation; personality changes Headaches: may be localized or generalized N/V: pressure on the medulla, stimulation of CTZ Papilledema: compression of the 2nd cranial nerve (optic), pressure on the central retinal vein; also known as choked disc

CLINICAL MANIFESTATIONS CONTD.

Seizures Localized manifestations: destruction, irritation, compression of the part of the brain in or near the tumor

Location Frontal lobe

Manifestations Disturbed mental state, apathy, inattentiveness, impaired long-term memory, abstraction difficulty, motor disorders Receptive aphasia, ataxia, tinnitus, generalized psychomotor seizures, recent memory impairment Sensory deficits, agnosia, dyslexia, right/left disorientation Headache, homonymous hemianopia, cortical blindness, seizures, hallucinations Unsteady gait, falling, ataxia, incoordination, CSF obstruction/hydrocephalus Vertigo, dizziness, vomiting, sudden death from respiratory/cardiac failure Hormonal dysfunction, sleep disturbances, water imbalance, temperature fluctuations, Cushings Syndrome Obstruction of CSF circulation, hydrocephalus, postural headache

CLINICAL MANIFESTATIONS
Temporal lobe

Parietal lobe Occipital lobe Cerebellar

Brain stem Pituitary and hypothalamus

Ventricle

MEDICAL MANAGEMENT
Managing increased ICP Controlling or preventing seizures Monitoring for motor and sensory deficits and cranial nerve deficits

SURGICAL MANAGEMENT
Biopsy Total removal of the brain tumor by way of craniotomy Surgical resection: decrease tumor bulk, making other treatments and adjunctive therapeutic treatments more effective

Craniotomy:

surgically create an opening into the

skull

NURSING MANAGEMENT

Preoperative Care: routine assessment V/S, LOC, Orientation, ability to follow instructions, PERRLA, extraocular eye movements, cranial nerve function Limb strength and movement Glasgow Coma Scale Postoperative Care Closely assess for injury to and edema of brain Monitor for increased ICP, motor/sensory deficits, cranial deficits, seizures, CSF leak, wound infection, CNS infections

TRANSPHENOIDAL HYPOPHYSECTOMY
To remove small tumors housed in the sella turcica (bony structure housing the pituitary gland) Fat or muscle grafts using tissue from the abdomen or upper thigh, are implanted at the surgical site to assist in healing of the hypophysectomy operative wound

POSTOPERATIVE CARE FOLLOWING PITUITARY SURGERY Frequent oral hygeine Cool vaporizer to keep oral mucous membranes moist Assess nasal drip pad for blood and CSF IV vasopressin or inhalation desmopressin for resulting Diabetes Insipidus (decreased secretion of ADH)

MEDICAL MANAGEMENT
Radiation therapy Chemotherapy

Nitrosoureas:
Carmustine

most frequently used and effective chemotherapy agent for brain tumors
(BCNU) Lomustine (CCNU)

Tic Douloureux

TRIGEMINAL NEURALGIA

TIC DOULOUREUX
Sensory disorder of the 5th CN Chronic irritation of the fifth cranial nerve Results in severe, recurrent, sharp facial pain along the trigeminal nerve Most common in ages 50-70 3 divisions of trigeminal nerve:

Opthalmic Maxillary Mandibular

ETIOLOGY
Gross abnormalities of the axon or myelin, as with multiple sclerosis Mechanical compression by tumors, vascular anomalies, dental abscesses, jaw malformation

TIC DOULOUREUX CONTD.

Characterized by intermittent episodes of intense pain of sudden onset Rarely relieved by analgesics Tactile stimulation may trigger an attack More prevalent in the maxillary and mandibular areas and on right side of the face; bilateral may also occur Pain can become so intense that client may ponder suicide

ASSESSMENT
Pain on the lips, gums, or nose, or across the cheeks Situations that stimulate symptoms: cold, washing the face, chewing, or foods or fluids of extreme temperatures

MANAGEMENT

Anticonvulsants: Carbamazepine (Tegretol); dampen reactivity of neurons within the trigeminal nerve Monitor liver enzymes during anticonvulsant therapy (liver impairment may result) Antispasmodic: Baclofen (Lioresal) may be used alone or in conjunction with anticonvulsants Emotional support Opioids not particularly effective Surgery: Nerve blocks with alcohol and glycerol (may provide relief of pain for up to 16 months) Peripheral neurectomy Percutaneous radiofrequency wave forms that create lesions that alter pain transmission Microvascular decompression; Rhizotomy: resection of the nerve root (both require craniotomy to access nerve)

NURSING INTERVENTIONS
Instruct client to avoid hot or cold foods and fluids. Provide small feedings of liquid and soft drinks. Instruct the client to chew the food on the unaffected side. Administer meds as prescribed.

PARKINSONS DISEASE

PARKINSONS DISEASE
Degeneration of dopamine-producing cells in the substantia nigra lead to degeneration of neurons in the basal ganglia (usually after age 60) Imbalance between dopamine and acetylcholine; dopamine inhibits excitatory impulses 3 cardinal features

Pin-rolling (tremors) Cogwheel

rigidity Bradykinesia/akinesia

MANIFESTATIONS

Generalized feeling of stiffness Mild, diffuse muscle pain Akinesia Shuffling gait Stooped posture Masklike facial expression Slow speech pattern, low volume, monotonous tone, poor articulation Involuntary drooling due to decreased swallowing reflex Decreased lacrimation Heat intolerance excessive perspiration

MEDICAL MANAGEMENT

Levodopa-Carbidopa Therapy: synthetic precursor of dopamine for basal ganglia Anticholinergic: Cogentin, Artane, Symmetrel; inhibit cerebral motor impulses that cause rigidity of the musculature MAOI: Bomcriptine, Parlodel; inhibit breakdown of dopamine Physiotherapy: decreased rigidity of muscles and prevents contractures Surgery: destroy globus pallidus (relieve rigidity) and/or thalamus (relieve tremors)

NURSING MANAGEMENT

Safe environment Nutrition: small pieces of food; small frequent meals; adequate intake of fiber to prevent constipation Positioning and activities: limit postural activities, maintain gait as normal as possible, may use cane or walker, encourage daily physical therapy to limit rigidity and prevent contractures Medical compliance Avoid rushing patient to move Assist in improvement of self-esteem Total body function support in advanced stages

MYASTHENIA GRAVIS

MYASTHENIA GRAVIS

Disturbance in the transmission of impulses at the myoneural junction resulting in profound weakness (eye muscles, eyelid, muscles of chewing, swallowing, speaking and breathing)

MANIFESTATIONS

Subjective Extreme muscle weakness, worsens as the muscle is used but disappears with rest; dysphagia; diplopia; dysarthria Objective Ptosis; dysphonia; Myasthenic smile (nasal smile); strabismus Diagnostic Test Neostigmine (Prostigmine) Subcutaneous or IV administration of Tensilon (prevents enzymatic breakdown of Acetylcholine): to provide relief of symptoms

MEDICAL MANAGEMENT
Pharmacologic: Acetylcholinesterase blockers; corticosteroids Plasmapheresis: clean up the blood

Myasthenic Crisis: undermedication leading to sudden inability to swallow or maintain respiration Cholinergic Crisis: overdose of anticholinesterase drugs

GUILLAIN-BARRE SYNDROME

Autoimmune following respiratory or GI infection, viral infection, viral immunization or surgery; areas of demyelination in the motor cells of the SC and medulla; ascending loss Versus ALS: descending loss Subjective: generalized weakness, paresthesia, diplopia Objective: ascending paralysis within the body usually 24-72 hours; respiratory paralysis; hypertension; tachycardia; low grade fever; incontinence Medical Management: steroids, plasmapheresis, support of vital functions Nursing Management: supportive care

MULTIPLE SCLEROSIS
Autoimmune response prior to viral infection Inflammation destroys myelin which leads to axon dysfunction; neurons in the SC, brain stem, cerebrum, cerebellum, and optic nerve are affected Stressors trigger MS Usually with adult females aged 20-40 years

MULTIPLE SCLEROSIS

Manifestations
Fatigue Optic

nerve involvement: blurred, hazy vision Brain stem involvement: nystagmus, dysarthria, cognitive dysfunctions, vertigo, deafness Weakness. Numbness in legs, spastic paresis, bladder and bowel dysfunctions Cerebellum: nystagmus, ataxia, hypotonia Blindness

MENINGITIS
Inflammation of the meninges Can spread rapidly Bacterial, viral, fungal, parasitic Bacterial: N. meningitidis, meningococcus, streptococcus pneumoniae, H. influenzae, E. coli Manifestations: fever, chills, headache, back and abdominal pain, N/V, nuchal rigidity, (+) Brudzinskis and Kernigs Signs, photophobia

MENINGITIS CONTD.
Viral: less severe, short duration, intense headache and malaise, N/V, lethargy, signs of meningeal irritation Encephalitis: acute inflammation of parenchyma of brain and SC Medications: antibiotics for 7-21 days, according to culture results; dexamethasone to relieve inflammation

HEALTH PROMOTION
Vaccination Prophylaxis Mosquito control Prompt diagnosis and treatment of clients with infection Asepsis in care of clients with open head and neurosurgery

HOMEWORK

Etiology, Clinical Manifestations, Medical/Surgical Management, Nursing Management Hydrocephalus Encephalocele Myelomeningocele Cerebral Palsy Reye Syndrome Short Bondpaper (1 margin on all sides; max. font 12; Arial, Book Antiqua, Times New Roman, or Calibri) Stapled Minimum 3 Reference Books not earlier than 2005 Deadline: July 19, 2010

VISUAL PROBLEMS

VISUAL IMPAIRMENT IS MORE THAN A PHYSIOLOGIC DEFICIT. Physical, emotional, and spiritual effects Even minor changes in vision can provoke feelings of anger and frustration in people who must rely on clear and sharp vision in their work Permanent and profound loss of vision can result in morbid grieving Loss of vision is a threat to persons independence, self-esteem, and self-control

VISUAL IMPAIRMENT
A common problem during childhood In the US the prevalence of blindness and serious visual impairment in the pediatric population is estimated at 30-64 per 100,000 population; another 100 children per 100,000 has less serious impairment

CLASSIFICATION

Visual impairment is a general term that refers to visual loss that cannot be corrected with regular prescription lenses.

School vision (a.k.a. Partially Sighted) refers to visual acuity between 20/70 and 20/200; child should be able to obtain an education in the usual public school system with the use of normal size print; near vision better than distance vision Legal blindness, visual acuity of 20/200 or less and/or visual field of 20 degrees or less in the better eye; allows special considerations with regard to taxes, entrance to special schools, eligibility for aid, and other benefits

ETIOLOGY
Can be caused by a number of genetic and prenatal or postnatal conditions Perinatal infections (herpes, chlamydia, gonococci, rubella, syphilis, toxoplasmosis) Retinopathy of prematurity Trauma Postnatal infections (meningitis) Disorders such as sickle cell disease, juvenile rheumatoid arthritis, Tay-Sachs disease, alibinism, and retinoblastoma

ETIOLOGY CONTINUED

Refractive errors are the most common types of visual disorders in children Trauma
Penetrating

wounds caused by sharp instruments Nonpenetrating wounds caused by foreign objects in the eyes, lacerations, a blow from a blunt object such as a ball

Infections
Conjunctivitis:

most common eye infection

ASSESSMENT
Assessment of children for visual impairment is a critical nursing responsibility. Discovery of visual impairment as early as possible is essential to prevent social, physical, and psychologic damage to the child.

ASSESSMENT CONTINUED
Identify those children who by virtue of their history are at risk Observe for behaviors that indicate a vision loss Screen all children for visual acuity and signs of other ocular disorders such as strabismus

INFANCY
Observe the neonates response to visual stimuli, such as following a light or object and cessation of body movement Lack of eye contact from the infant must be taken seriously Test infant for strabismus Lack of binocularity after 4 months of age is considered abnormal and must be treated to prevent amblyopia

CHILDHOOD
Refractive errors are common, so test for visual acuity School nurse is usually responsible for vision testing in schoolchildren

CONGENITAL CATARACTS

Opacity of crystalline lens

CONGENITAL CATARACTS

Pathophysiology: prevents light rays from entering eye and refracting on retina

CONGENITAL CATARACTS

Clinical Manifestations

Gradually less able to see objects clearly May lose peripheral vision Nystagmus (with complete blindness) Gray opacities of lens Strabismus Absence of red reflex Requires surgery to remove cloudy lens and replace lens (intraocular lens implant, removable contact lens, prescription glasses) Must be treated early to prevent blindness from amblyopia

Treament

STRABISMUS
squint or cross-eye Malalignment of eyes Estropia: inward deviation of eye Exotropia: outward deviation of eye

STRABISMUS

Pathophysiology
May

result from muscle imbalance or paralysis, poor vision, or congenital defect Because visual axes are not parallel, brain receives two images, and amblyopia can result

STRABISMUS

Clinical Manifestations
Squints

eyelids together or frowns Has difficulty in focusing from one distance to another Inaccurate judgment in picking up objects Unable to see print or moving objects clearly Closes one eye to see Tilts head to one side Diplopia; Photophobia; Dizziness; Headache; Cross-eye

STRABISMUS

Treatment
Depends

on cause of strabismus May involve occlusion therapy (patching stronger eye) or surgery to increase stimulation to weaker eye Early diagnosis is essential to prevent vision loss

RETINOBLASTOMA
Most common congenital malignant intraocular tumor of childhood Approx. 11 cases per million in children younger than 5 years of age Caused by a mutation in a gene and may occur sporadically or be inherited Develops when a mutated gene is unable to produce the natural signals to stop the growth of retinal cells

RETINOBLASTOMA CONTINUED

Of all cases, the majority are nonhereditary and unilateral Hereditary retinoblastomas are transmitted as an autosomal dominant trait with a 90% penetrance

DIAGNOSTIC EVALUATION

Parents first observe a whitish glow in the pupil, known as the cats eye reflex (white reflex) or leukokoria Leukokoria: visualization of the tumor as the light momentarily falls on the mass Refer eye abnormalities, such as cats eye reflex, strabismus, decreased vision, and persistent painful erythematous eyes, to opthalmologist Definitive diagnosis: opthalmoscopic examination under general anesthesia Imaging studies, including ultrasonography and computed tomography of the orbit, are done to determine the extent of the disease.

THERAPEUTIC MANAGEMENT
Aim of therapy: to preserve useful vision and eradicate the tumor Treatment depends chiefly on the stage of the tumor at the time of the diagnosis Reese-Ellsworth classification: commonly used standard for intraocular disease; for staging of retinoblastoma (Group I, Very Favorable; Group II, Favorable; Group III, Doubtful; Group IV, Unfavorable; Group V, Very Unfavorable)

THERAPEUTIC MANAGEMENT CONTINUED Recent shift away from the use of external beam radiation, which damages the cells DNA Towards FOCAL INTRAOCULAR therapy with or without chemotherapy Some common focal therapies:

Plaque

brachytherapy: surgical radioactive implant on the sclera until maximum dose has been delivered to the tumor

THERAPEUTIC MANAGEMENT CONTINUED

Some focal therapies continued

Laser

photocoagulation: laser beam to coagulate blood supply to the tumor Cryotherapy: freezing the tumor by destroying the microcirculation to the tumor through microcrystal formation Thermotherapy: uses microwaves or infrared radiation to deliver heat to the tumor

THERAPEUTIC MANAGEMENT CONTINUED Chemotherapy: to reduce tumor size to facilitate focal intraocular treatment (chemoreduction) Chemoreduction and chemoprevention include 2-6 courses of vincristine, etoposide, and carboplatin, with or without cyclophosphamide Chemoreduction reduces risk of radiation induced malignancies and facial disfigurement

THERAPEUTIC MANAGEMENT CONTINUED With advanced tumor growth and no hope for useful vision, enucleation of the affected eye is the treatment of choice After enucleation, the orbital implant is placed to provide a more natural cosmetic appearance, minimizes sinking of the prosthetics, and enables motility of the prosthesis

THERAPEUTIC MANAGEMENT CONTINUED

With bilateral disease, every attempt is made to preserve useful vision in both eyes Trilateral retinoblastoma is a rare, usually fatal syndrome; comprises of bilateral retinoblastoma with the involvement of the pineal gland tumor or other midline structure Aggressive chemotherapy, radiation therapy, adjuvant treatments, and gamma knife therapy with little success Longer survival with early diagnosis and use of initial chemoreduction upon diagnosis

PROGNOSIS
Overall prognosis is very favorable Of long-term concern is the development of decreased visual acuity, facial disfiguration, and secondary tumors Children with bilateral disease are more likely to develop secondary cancers Chemoprevention and high-dose chemotherapy with autologous stem cell rescue, beneficial to patients with metastatic retinoblastoma

NURSING CONSIDERATIONS

If parents report noticing a strange light in the eye or expression, these concerns must be taken seriously. Follow-up families with history Educate parents about indirect opthalmoscopy, which is the diagnostic procedure After procedure, child may not see very clearly, or eyes may be sensitive to light due to pupillary dilation; parents should be aware of these normal reactions Bone surveys and bone marrow aspiration are rarely performed unless metastatic disease is suspected

NURSING CONSIDERATIONS CONTINUED

After disease is staged, practitioner confers with the parents regarding treatment For extensive disease, enucleation is the treatment of choice After surgery, parents are prepared for childs facial appearance: eye patch, face may be edematous or ecchymotic Parents often fear seeing the surgical site because they imagine a cavity in the skull A surgically implanted sphere maintains the shape of the eyeball, and the implant is covered by the conjunctiva. When the lids are open, the exposed area resembles the mucosal lining of the mouth.

NURSING CONSIDERATIONS CONTINUED After the child is fitted for a prosthesis, usually within three weeks, the facial appearance returns to normal. Care of the socket is minimal and easy to accomplish; wound is clean and has little or no drainage Antibiotic ointment, irrigating solution, and daily dressing is necessary until after the socket has healed completely

PHYSICAL EXAMINATION: EXTERNAL EYE

Eye position: symmetry, alignment Eyebrows: symmetry, hair distribution, skin conditions, movement Eyelids and Eyelashes: placement and symmetry

Ptosis: due to aging or to edema, 3rd cranial nerve disorders, neuromuscular disorders Entropion and ectropion can result in corneal irritation Inspect upper and lower lids Palpate: texture, firmness, mobility, integrity of underlying tissues

PE: EXTERNAL EYE CONTD.

Blink Response involuntary reflex that occurs bilaterally up to 20 times a minute Eyeballs palpate for firmness and symmetry Lacrimal Apparatus Retract upper lid and have client look down so that part of the lacrimal gland can be visualized Observe area for swelling or tenderness Inspect area over lower lid and nose for edema Palpate area over lower orbit rim near the inner canthus; should have no regurgitation of fluid from the sac

PE: EXTERNAL EYE CONTD.

Conjunctivae and Sclerae

Inspect:

healthy conjunctivae are pink to light

red

Corneal Reflex
Performed

to assess function of trigeminal nerve

Cornea
Inspect

cornea from oblique angle while shining a penlight on the corneal surface: the irises should be easily visible Arcus senilis: a thin, grayish white ring around the edge of the cornea may be seen in older

PE: EXTERNAL EYE CONTD.

Anterior Chamber Inspect anterior chamber while observing the cornea Chamber should appear clear and transparent with no cloudiness or shadows cast on the irises Depth between cornea and iris is normally about 3mm; shallower or deeper chambers should be referred to ophthalmologist Iris and Pupil Iris should have consistent color PERRLA

PE: EXTERNAL EYE CONTD.

Ocular motility

Assess 6 cardinal directions of gaze: speed, smoothness, range, symmetry Shine penlight at bridge of clients nose from a distance of 12-15 inches while client stares straight ahead; observe for symmetrical light reflections on both corneas; assymmetry may reflect strabismus Observe uncovered eye for median or lateral movement as it focuses on a fixed point

Corneal Light Reflex Test/Hirschbergs Test

Cover-Uncover Test

PE: EXTERNAL EYE CONTD.

Visual Acuity
Use

of Snellen Chart Results expressed as a fraction Numerator denotes the distance the client is from the chart letters, and the denominator denotes the distance from the chart at which a client with normal vision can see the chart letters

Visual Fields
Confrontational

method or with computerized

instrument

PHYSICAL EXAMINATION: INTERNAL EYE

Visible only with the use of an ophthalmoscope Direct Ophthalmoscopy Red reflex: bright red-orange glow seen through the pupil Optic disc round with well-defined margins Retinal veins darker than arteries and radiate from the disc Tortuous vessels or straightened arteries are abnormal Indirect Ophthalmoscopy Provides for direct visual inspection with depth perception and permits a wider field of view compared to the direct method

PE: INTERNAL EYE CONTD.

Tonometry Method of measuring intraocular fluid pressure with the use of calibrated instruments that indent or flatten the corneal apex Hand-held tonometer Cornea is anesthetized; client sits and looks straight forward; tonopen is held perpendicular to the cornea and tapped several times directly on the cornea; a computer chip in the instrument averages the readings and notes the standard deviation Applanation tonometer Either hand-held or attached to a slit-lamp microscope; measures amount of force required to flatten the corneal apex by a standard amount

PE: EXTERNAL EYE CONTD.

Slit-Lamp Examination Slit-lamp microscope used to illuminate and examine the anterior segment of the eye under magnification A linear slit beam of incandescent light is projected onto the globe, illuminating an optical cross-section of the anterior chamber Client sits, and the head is stabilized by an adjustable chin rest and forehead strap Fluorescein dye used to highlight corneal irregularities Other devices that may be attached:
Gonioscope: provides visualization of the anterior chamber angle Hruby lens: examination of the vitreous body and fundus Pachymeter: to measure thickness of cornea and the anterior chamber

DIAGNOSTIC TESTS

Fundus Photography Special retinal cameras used to document fine details of the fundus for study and future comparison Exophthalmometry To measure forward protrusion of the eye Ophthalmic Radiography To evaluate orbital and intracranial conditions Neoplasms, inflammatory masses, fractures, and extraocular muscle enlargement MRI To image edema, areas of demyelination, vascular lesions

DIAGNOSTIC TESTS CONTD.

Ultrasonography
A-scan:

to measure axial length, distance from cornea to retina, and to determine refractive power of intraocular lens in cataract surgery B-scan: to evaluate characteristics of a lesion

Ophthalmodynamometry
Gives

an approximate measurement of the relative pressures in the central retinal arteries and indirectly assesses carotid arterial flow on either side

DIAGNOSTIC TESTS CONTD.

Electroretinography
To

evaluate integrity of the retina Retinal diseases evaluated: retinitis pigmentosa, massive ischemia, disseminated infection, toxic effects from drugs or chemicals

Visual Evoked Response

Also

measures electrical potential resulting from a visual stimulus Retinal or optic nerve disease can be diagnosed

DIAGNOSTIC TESTS CONTD.

Fluorescein Angiography
Small amount of fluorescein dye is injected into antecubital vein Dye passes through retinal and choroidal circulation, it can be visualized and photographed Photos may demonstrate leakage of dye from abnormal vessels After examination: encourage increased oral fluid intake; during next 24 hours, urine will be yellowish and jaundice in light-complexioned clients; dark glasses for several hours until pupils can constrict again

GLAUCOMA

Characterized by increased intraocular pressure, optic nerve atrophy, and visual field loss Blindness can be prevented if treatment is begun early

CLASSIFICATION

Primary Open-Angle Glaucoma

Most

common; genetically determined; bilateral; slow to progress Often referred to as the thief in the night because no early clinical manifestations are present to alert patient that vision is being lost

Angle-Closure Glaucoma
Can

develop only in an eye in which the anterior chamber angle is anatomically narrow

OTHER FORMS

Normal-tension Glaucoma
Resembles

primary open-angle glaucoma Optic nerve is damaged even though IOP is not high

Secondary Glaucoma
May

occur as a result of trauma that can disrupt the flow pattern of aqueous humor

ETIOLOGY AND RISK FACTORS

Most common cause of chronic open-angle glaucoma is degenerative change in the trabecular meshwork, resulting in decreased outflow of aqueous humor HPN, Cardiovascular Disease, DM, and obesity are associated in the development of glaucoma Family history History of systemic heart disease

PATHYPHYSIOLOGY
Increased IOP due to hyperproduction of aqueous humor or obstruction of outflow As aqueous fluid builds up in the eye, the increased pressure inhibits blood supply to the optic nerve and the retina, which becomes ischemic and gradually lose function

CLINICAL MANIFESTATIONS
Acute angle-closure and secondary glaucoma: Severe pain, blurred vision or vision loss; rainbow halos around lights; nausea and vomiting Loss of blood supply to the retina lead to visual field defects Opthalmoscopic examination: atrophy (pale color) and cupping (indentation) of the optic nerve head

CLINICAL MANIFESTATIONS

In chronic open-angle glaucoma, a small crescent-shaped scotoma (blind spot) appears early in the disease In acute angle-closure glaucoma, the field demonstrate larger areas of significant loss of vision Angle-closure glaucoma: erythematous conjunctiva and corneal cloudiness; aqeuous humor in the anterior chamber may also appear turbid, and pupil may be nonreactive; increased IOP (>23 mmHg) indicates the need for further evaluation Gonioscopy: to determine the depth of the anterior chamber angle and to examine the entire circumference of the angle for any abnormal changes in the filtering meshwork

GOAL OF MANAGEMENT
To facilitate outflow of the aqueous humor through remaining channels and to maintain IOP within a range that prevents further damage to the optic nerve If IOP is very high, it must be reduced to retain vision If vision is lost, the goal is to restore clients independence

MEDICAL MANAGEMENT
Reduce intraocular pressure (promote aqueous flow) Narrow-angle Glaucoma: topical mitotics or epinephrine to constrict pupils, which opens the canal of Schlemm and promotes drainage of aqueous humor Topical beta-blocker or alpha-adrenergic agents or oral carbonic anhydrase inhibitors: reduces production of aqueous humor

MEDICAL MANAGEMENT CONTINUED

In emergent situations, an oral osmotic diuretic (glycerin {Osmoglyn}) may be administered. Diabetic clients often receive a synthetic glycering such as isosorbide to reduce the effect on blood glucose levels IV mannitol may be used to arrest extremely high IOP

SURGICAL MANAGEMENT

Laser trabeculoplasty: to create an opening in trabecular meshwork; effect of treatment decreases with time, and procedure may need to be repeated Trabeculectomy: creation of an opening through which the aqueous fluid escapes Filtering procedures: operations such as trephination, thermal sclerostomy, and sclerectomy create an outflow channel from the anterior chamber into the subconjunctival space; aqueous humor is absorbed Iridectomy: creates opening in the iris for a new route for flow of aqueous humor Cyclocryotherapy (application of a freezing tip) or cyclophotocoagulation: to destroy ciliary body and decrease production of aqeuous humor

NURSING PROCESS

Assessment Demographic data of age and race because openangle glaucoma occurs most often in clients over 40 and in blacks Family history Accurate list of current medications, including OTC drugs Allergies, particularly to medications Ask client to describe any changes in vision: blind spots in the periphery, overall decreased visual acuity, loss of contrast sensitivity

NURSING PROCESS CONTINUED

Nursing Diagnoses
Disturbed

sensory perception Anticipatory grieving Risk for ineffective therapeutic regimen management Risk for infection (postoperative)

CATARACTS

Cataract is opacity of the lens Some degree of cataract formation is to be expected in most people over 70 years of age Worldwide, it is the primary cause of reduced vision and blindness

SENILE CATARACTS

Most common type is the age-related or senile type Usually begin around the age of 50 years Cortical cataracts: spoke-like opacifications are found in the periphery of the lens; progress slowly and often do not cause severe loss of vision Nuclear sclerotic cataracts: result of a progressive yellowing and hardening of the central lens (nucleus) Posterior subcapsular opacities: occur centrally on the posterior lens capsule and cause visual loss early in their development

ETIOLOGY AND RISK FACTORS

Cumulative exposure to UV light over a persons life span High altitude Working in bright sunlight Welders who do not wear eye protection Systemic disorders: diabetes, tetany, myotonic dystrophy, neurodermatitis, galactosemia, Lowes, Werners and Down syndrome Intraocular disorders: iridocyclitis, retinitis, retinal detachment, onchocerciasis Infections in the first trimester of pregnancy may cause congenital cataracts Blunt trauma, lacerations, foreign bodies, radiation, exposure to infrared light, chronic use of corticosteroids

PATHOPHYSIOLOGY
Cataract formation: reduction in oxygen uptake and an initial increase in water content followed by dehydration of the lens Sodium and calcium contents are increased Potassium, ascorbic acid, and protein contents are decreased Photochemical process: Protein in the lens undergo age-related changes along with photoabsorption of UV radiation throughout life

PROGRESS OF CATARACTS
Immature cataracts that are not completely opaque and allow for useful vision

Mature cataracts are completely opaque; vision is significantly reduced

Hypermature cataracts: lens proteins break down into short-chain polypeptides that leak out through the lens capsule; pieces of protein are engulfed by macrophages, which may obstruct the trabecular meshwork, causing Phacolytic Glaucoma

CLINICAL MANIFESTATIONS

Blurred vision; Monocular diplopia (double vision); Photophobia; Glare Usually see better in low light, when pupil is dilated No pain complaint Cloudy lens can be observed Distorted or absent red reflex seen with direct opthalmoscope Type and extent of the lens change requires a slit-lamp examination

SURGICAL MANAGEMENT
Ripened cataract (dramatic visual impairment) is surgically removed with lens replacement Outpatient basis unless ocular complications or health factors occur Preoperative eyedrops: dilating agent, tropicamide (Mydriacyl); cycloplegic cyclopentolate (Cyclogyl), to paralyze ciliary muscles

SURGICAL REMOVAL OF CATARACT

Usually under topical anesthesia using eyedrops Small incision in the cornea
Cataract is broken into microscopic particles by phacoemulsification (high-energy sound waves) using ultrasonic probe

A folded IOL is inserted through the microincision, unfolded, and locked into permanent position

Small incision is self-sealing, requires no stitches, remains tightly closed by natural outward pressure within the eye

COMPLICATIONS
Secondary glaucoma due to postoperative edema in the ocular tissues Expected elevation in the IOP resolves within 24-72 hours Postoperative infection, bleeding, macular edema and wound leaks Incidence of retinal detachment high within first 12 months after cataract surgery

NURSING MANAGEMENT
Assessment: risk factors; visual acuity; ask to describe visual disturbances; assess perception of quality of vision to determine need for surgery Diagnosis: Disturbed Sensory Perception Outcome: Improved visual perception evidenced by improved vision or adaptation to changes in visual acuity

NURSING MANAGEMENT CONTINUED

Interventions: based on assisting client to gain or maintain as much independence as possible Evaluate lifestyle, abilities, and home environment After cataract surgery: return for follow-up visit the next morning and again at 1 week and at 1 month Nausea and vomiting should be reported immediately because prolonged vomiting may increase IOP and cause wound dehiscence Eye patch is usually removed the next morning Assess ability to instill eye drops appropriately

CARE AFTER CATARACT REMOVAL

Leave eye patch in place Limit activity for 24 hours Do not rub eye May wear glasses Avoid lifting (approx. >2 kg) and straining Do not sleep on the side of body that was operated on Take eye drops and acetaminophen prn for pain or itching DO NOT take aspirin or drugs containing aspirin Report unrelieved pain, redness around the eye, nausea or vomiting Wear eye shield to protect eye

ERRORS OF REFRACTION
Exist when light rays are not focused appropriately on the retina of the eye Optical correction to distinguish between visual loss caused by disease and visual loss caused by refractive error Refractometry: measurement of refractive error

MYOPIA

a.k.a. nearsightedness Light rays come into focus in front of the retina The refractive power of the eye is too strong and a CONCAVE, or minus, lens is used to focus light rays on the eye Mostly caused by a longer-than-normal eyeball, which may be a familial trait Transient myopia may occur with administration of medications or associated with disorders such as influenza, typhoid fever, severe dehydration, and large intakes of antacids

HYPEROPIA
a.k.a. farsightedness Light rays come into focus behind the retina CONVEX, or plus, lens is used to correct vision Usually caused by an eyeball that is shorter than normal or a cornea that has less curvature than normal Adults are more often affected than children Demands for close work and reading usually bring on manifestations of headache or eyestrain

ASTIGMATISM
Light rays are not bent equally by the cornea in all directions so that a point of focus is not attained Mostly because the curvature of the cornea is not perfectly spherical Poor vision for both distant and near objects Corrected with cylindrical lens

SURGICAL MANAGEMENT

Laser in situ keratomileusis (LASIK): an extremely thin layer of the cornea is peeled back for the laser reshaping on the middle layer of the cornea and then put back in place
Little

postoperative discomfort, rapid recovery of clear vision, quick stabilization of refractive change 10-15 minutes; outpatient basis High success rate; low complication rate

SURGICAL MANAGEMENT CONTINUED

Excimer laser photorefractive keratectomy (PRK): uses short-wavelength, high-energy ultraviolet radiation lasers to reshape the corneal surface; flattened for myopia; making the central corneal curvature steeper to correct hyperopia Outpatient basis Usually takes 30 minutes, which is mostly teaching client to keep eye still; Actual treatment takes less than a minute Longer and more painful recovery Vision will be reduced for several days after surgery

SURGICAL MANAGEMENT CONTINUED

Radial keratotomy (RK): involves making tiny cuts in the cornea, which flatten it to reduce nearsightedness; in people who have both astigmatism and myopia, the surgeon may make additional cuts to flatten the misshapen part of the cornea that is causing the astigmatism Outpatient basis; under local or topical anesthesia Entire process is usually less than 2 hours (preparation time, postoperative care, paperwork) Successful and safe for mild to moderate

SURGICAL MANAGEMENT CONTINUED

Corneal Implants
Clear

pieces of acrylic that can be surgically implanted into the cornea Implants flatten the cornea and reduce nearsightedness Very effective for correcting mild nearsightedness

NURSING MANAGEMENT OF THE SURGICAL CLIENT Eye protection postoperatively Avoid vigorous activities, activities that could get water in the eye, and eye make-up Steroids to reduce inflammation Most clients report watering of eyes and minimal pain Refraction slowly stabilizes after surgery Reduced contrast sensitivity in night vision and daytime glare is common

CORNEAL INFECTION: KERATITIS

Dry eyes or ineffective eyelid closure predisposes the eye to keratitis Systemic collagen disoders, such as rheumatoid arthritis, are particularly susceptible to corneal infections and ulcerations Clinical manifestations: excess tearing, pain worsened by eyelid movement, sensitivity to light, indurated sclera; blurred vision results from inability of cornea to provide proper refractive surface

KERATITIS
May develop into ulcerations that severely compromise the integrity of the eye Sources of infection: bacteria, viruses, protozoa Hypopyon, a layer of white cells in the anterior chamber, may accompany corneal ulcerations

OUTCOME MANAGEMENT

Goal: to eradicate infection, prevent further injury to the cornea, and promote comfort and healing Medical Management: topical antibiotic, antifungal, and antiviral therapy Surgical Management Tarsorrhaphy (suturing eyelid closed) promotes healing by decreasing eyelid blinking and by decreasing evaporation of the corneal tear film For corneal perforation, a conjunctival flap may be performed to cover the defect

OUTCOME MANAGEMENT CONTINUED

Surgical Management Tissue adhesive may be used to seal the perforation Soft contact lens may be used as bandage to maintain the seal Large perforation: either lamellar (partial-thickness) or penetrating (full-thickness) keratoplasty When medical and surgical interventions fail, enucleation (removal or entire eyeball), or in some cases, evisceration (removal of orbital contents) may be indicated

NURSING MANAGEMENT
Early stages of corneal infection are often managed at home Hospitalization for severe corneal ulcer Assess clients level of discomfort and methods of coping with the stress of pain and lack of sleep Hand-washing when instilling eye drops, even if gloves are worn; strict adherence to time schedule

NURSING MANAGEMENT CONTINUED

Frequent cleaning may be needed because medications and excessive tears will become dried and the lids will stick together Warm tap water, applied with soft gauze pads, is used To avoid skin excoriation, antibiotic ophthalmic ointment may be applied to the lower lid margin and cheek to reduce irritation

NURSING MANAGEMENT CONTINUED

Outline daily routine of care and identify periods to allow client to rest Speak to client before touching him or her Oral analgesics and mild sleeping medications at bedtime Frequency of eyedrops instillation is reduced from q 15 mins to q 30 mins, to q hour

SELF-CARE
Assess ability to instill eyedrops properly Educate client about importance of complying with medication regimen Instruct client and family about clinical manifestations of increasing infections Eye may continue to be cleaned with warm tap water at home Assess home environment if vision is greatly reduced make referrals if necessary

HORDEOLUM (STYE)
Infection of glands of eyelids Redness and swelling of localized area of the eyelid Management:

Warm

compresses and antibiotics May need to be incised and drained

BLEPHARITIS
Chronic, bilateral inflammation of eyelids Itching and burning of the eyes, eyes appear red, scales noted on the lashes Management:

Wash

eyelids with baby shampoo, water, and cotton-tipped applicators Antibiotic ointments may be prescribed

CONJUNCTIVITIS
Inflammation of conjunctiva from various microorganism Redness, tearing, and exudation of eyelid May progress to eyelid drooping, abnormal tissue growth Management:

Antibiotic eyedrops

PTOSIS
Drooping of eyelid from several causes Irritation of eye caused by drying, loss of tears Management:

Artificial

tears Surgical correction needed Sometimes glasses used to lift redundant skin

LAGOPHTHALMOS
Inadequate closure of eyelids Irritation of eye caused by drying Management:

Artificial

tears Eye shields at night Surgical correction

ABSENCE OF BLINKING
Lack of blinking seen with Parkinsons disease and hyperthyroidism Blinking fewer than 20 times a minutes Management:

Artificial

tears Eye shields at night

RETINAL DETACHMENT
Separation of the retina from the choroid, a membrane dense with blood that is located between the retina and the sclera Rhegmatogenous retinal detachment: most common; due to a retinal hole; vitreous fluid seeps through hole and separates retina from its blood supply; detachment spreads over a period of hours to years

PREDISPOSING FACTORS

Aging Cataract extraction Degeneration of the retina Trauma Severe myopia Previous retinal detachment in the other eye Family history

CLINICAL MANIFESTATIONS

Described by clients as a shadow, black areas, or curtain falling across field of vision as a result of separation of visual receptors from the neural pathway No pain associated Onset usually sudden and may be accompanied by a burst of black spots or floaters indicating bleeding due to detachment Client may also see flashes of light caused by separation of the retina

CLINICAL MANIFESTATIONS CONTINUED Visual field loss occurs the opposite quadrant of the actual retinal detachment Giant retinal tears may result in temporary blindness Peripheral tears may not interfere with central vision at all Opthalmoscopic examination: areas of retinal detachment appear bluish gray as opposed to normal red-pink color

SURGICAL MANAGEMENT
Goal: to place retina back in contact with choroid and to seal accompanying holes and breaks General anesthesia Pupil widely dilated before operation May take several hours

SURGICAL MANAGEMENT CONTINUED

Laser Photocoagulation: if retina is torn or slightly detached, laser can be used to burn the edges of the tear and halt progression; if detachment is small, laser can seal retina against the choroid; outpatient under local anesthesia Cryoprexy: uses nitrous oxide to freeze tissue behind retinal tear, stimulating scar tissue formation that will seal the edges of the tear; outpatient under local anesthesia

SURGICAL MANAGEMENT CONTINUED

Pneumatic Retinopexy: eye is numbed with local anesthesia and a small gas bubble is injected into the vitreous body; the bubble rises and presses against the retina, pushing it against the choiroid; the gas bubble is slowly absorbed over the next 1 or 2 weeks Scleral Buckling: sclera is depressed from the outside by rubber-like silicone sponges or bands that are sutured permanently; in addition, an intraocular injection of air or sulfur hexafluoride gas bubble to apply pressure on the retina from the inside of the eye

NURSING MANAGEMENT

Focus on helping the client cope with the fears and reality of loss of vision and to adapt to changes in vision Client must be aware of clinical manifestation of loss of vision Post-op: observe eye patch for any drainage, normally serous; assess level of pain and presence of nausea Activity restrictions for air or gas bubble injection; positioning in favor of force of gravity (use pillows for support) For scleral buckling, opioids may be needed during first 24 hours after surgery; nausea and vomiting may also require management

NURSING MANAGEMENT CONTINUED

IV acetazolamide (Diamox) may be used to reduce increased IOP, which is monitored closely for the first 24 hours. Regular diet and fluids as tolerated Eye patch removed the next morning Redness and swelling of lids and conjunctiva expected due to surgical manipulation Conjunctiva may remain red or pink for a few weeks Post-op medications: antibiotic-steroid combination eyedrop to prevent infection and reduce inflammation Cycloplegic agents to dilate pupil and relax ciliary muscles Warm or cold compresses for comfort several times a day

SELF-CARE
Clean eye with warm tap water using clean washcloth Warm compresses may be continued at home Eye shield or glasses during the day; shield during naps and at night Avoid vigorous activities and heavy lifting during immediate postoperative period If with air and gas injection, avoid air travel as they expand in high altitudes

DIABETIC RETINOPATHY
One of the leading cause of blindness worldwide Progressive disorder of the retina characterized by microscopic damage to the retinal vessels, resulting in occlusion of the vessels; as a result, sections of the retina deteriorate and vision is permanently lost

CLASSIFICATION

Background/Nonproliferative Retinal vessels are hyperpermeable and weak Multiple hemorrhages occur from these defective vessels Retinal edema is caused by leaking capillaries Hemorrhages, exudates, ischemia contribute to impaired vision Proliferative Progressive retinal ischemia stimulates growth of new but ineffective blood vessels which proliferate and grow into the vitreous body Leaks, hemorrhages, fibrous changes may form bands that pull on the retina and cause detachment

CLINICAL MANIFESTATIONS
spiders, cobwebs, or tiny specks floating in their vision Dark streaks or a red film that blocks vision Vision loss, usually in both eyes, but more so in one eye Blurred vision that may fluctuate Dark or empty spot in the center of vision Difficulty adjusting from bright light to dim light

OUTCOME MANAGEMENT

Photocoagulation Goal is to stop the leakage of blood and fluid in the retina and thus slow progression of diabetic retinopathy; high-energy laser creates small burns in areas of retina with abnormal blood vessels to seal any leaks Vitrectomy Removal of blood-filled vitreous; tissue is cut and removed piece by piece from the eye; volume of removed tissue is replaced with saline to maintain normal shape and pressure of the eye

NURSING INTERVENTIONS
Vision will be blurry for about a day Mild pain, headache, sensitivity to light are expected and can be controlled by eye patch and OTC pain relievers Small spots caused by laser burns may appear in the visual field; they generally fade and disappear with time

AUDITORY AND SPEECH PROBLEMS

Common Health Problems of the Neonate and Infant

MUSCULOSKELETAL PROBLEMS

DEVELOPMENTAL DYSPLASIA OF THE HIP Developmental Dysplasia of the Hip (DDH): broad spectrum of disorders related to abnormal development of the hip that may develop at any time during fetal life Congenital Hip Displacement: onset during fetal development Incidence: 10/1000 live births; higher in Caucasians than other groups

ETIOLOGY AND PATHOPHYSIOLOGY

Cause is unknown But certain factors are believed to affect risk: gender, birth order, family history, intrauterine position, delivery type, joint laxity, and postnatal positioning Physiologic factors: includes maternal hormone secretion and intrauterine positioning Mechanical factors: breech presentation, multiple fetuses, oligohydramnios, and large infant size Genetic factors: higher incidence of DDH in siblings of affected infants