SENSORY-

PERCEPTUAL
DISORDERS

Eric B. Panopio, M.D.

 objectives:
 Describe the nature and properties of sensory and perceptual
components in the human body.
 Understand the pathophysiology behind sensoriperceptual
disorders.
 Assess effectively the client with sensory and perceptual
alterations.
Overview of the
Nervous System
 THE NEURON
 The Neuron is the Basic Functional Unit of the Nervous System.
 Whatever their specific function, all neurons have the same physical parts: The
Cell Body, Dendrites and One Axon.

Neurons can be classified into THREE TYPES:

 SENSORY (RECEPTOR) NEURONS (AFFERENT) - Carry impulses
from the SENSE ORGANS (RECEPTORS) to the Brain and Spinal Cord. 
Receptors detect external or internal changes and send the information to the
Central Nervous System in the form of impulses by way of the Afferent
Neurons.
 MOTOR NEURONS (EFFERENT) - Carry impulses from the Brain and
Spinal Cord to MUSCLES or GLANDS.  Muscles and Glands are Two Types
of Effectors.  In response to impulses, Muscles Contract and Glands Secrete.
 INTERNEURONS - Connect Sensory and Motor neurons and carry impulses
between them.  They are found entirely within the Central Nervous System
 CELL BODY - The largest part, contains the nucleus and
much of the cytoplasm (area between the nucleus and the cell
membrane), most of the metabolic activity of the cell,
including the generation of ATP (Adenine Triphosphate
Compound that Stores Energy) and synthesis of protein.
 DENDRITES - Short branch extensions spreading out from
the cell body.  Dendrites Receive STIMULUS (Action
Potentials) and carry IMPULSES from the environment or
from other NEURONS and carry them toward the cell body
 AXON - A Long Fiber that carries impulses away from the cell
body.  Each neuron has only ONE AXON.  The Axon Ends in
a series of small swellings called AXON TERMINALS.
 covered with a Lipid Layer known as the MYELIN SHEATH which
insulates & speeds up transmission of nerve impulses through the axon
 In the Peripheral Nervous System, Myelin is produced by SCHWANN
CELLS, which surround the Axon.
 GAPS (NODES) in the Myelin Sheath along the length of the Axon are
known as the NODES OF RANVIER
 Neuron
 Axon
 Dendrites
 Synapse
 Neurotransmitters
 Myelin sheath
Types of Neurons
Types of
Neuroglia
 Nervous System
 consists of the:
 Central Nervous System

 Peripheral Nervous System

 Autonomic Nervous System

 The Central Nervous System (CNS) consist of the Brain and the
Spinal Cord. The Spinal Cord carries messages from the body to the
Brain, where they are analyzed and interpreted.  Response Messages are
then passed from the Brain through the Spinal Cord and to the rest of the
Body.

 The Peripheral Nervous System (PNS) consists of the neurons NOT

Included in the Brain and Spinal Cord.  Some Peripheral Neurons
Collect Information from the Body and Transmit it TOWARD the
CNS.  These are called AFFERENT NEURONS.  Other Peripheral
Neurons Transmit Information AWAY from the CNS.  These are called
EFFERENT NEURONS.

 The Autonomic Nervous System (ANS), also known as the

"involuntary" nervous system controls activities of the body
unconsciously. It includes all the nerve cells, or neurons, located outside
the spinal cord and the brain stem. The Sympathetic division sends
impulses that speed up or enhance (as in running) whereas the
Parasympathetic division slows down (digestion). These two systems
combined regulate the majority of the body's involuntary functions.
 INCREASED
INTRACRANIAL
PRESSURE
 Increased Intracranial Pressure
Alternate Names:
 ICP
Definition
 A condition in which the pressure of the
cerebrospinal fluid or brain matter within the
skull exceeds the upper limits for normal
pressure.
Subdural Hematoma
 Causes & Risk Factors
 severe head injury
 battered child syndrome
 subdural hematoma
 intraventricular hemorrhage
 meningitis
 meningoencephalitis
 lead poisoning
 Reye's syndrome
 hypervitaminosis A
 diabetic ketoacidosis (during treatment)
 water intoxication (psychogenic polydipsia)
 decerebrate posture
 decorticate posture
 fontanelles - bulging
 Signs & Symptoms
Infants:
 bulging fontanelle
 separated sutures
Older children and adults:
 vomiting
 headache
 changes in behavior
 progressive decreased consciousness, may become
coma
 seizures
 Diagnosis & Tests
 N intracranial pressure: 8-12 mm Hg.
 Measured during a spinal tap (lumbar
puncture) or may be measured directly by
attaching a device referred to as a bolt to a
small hole in the skull.
 Treatment
 Close monitoring in the ICU
 Aggressive treatment
 Complications
 brainstem herniation
CEREBROVASCULAR
ACCIDENT
 Cerebrovascular Accident
Alternate Names :
 Cerebral Infarction, Cerebrovascular Disease, CVA
Definition
 A stroke is an interruption of the blood supply to any
part of the brain, resulting in damaged brain tissue.
 a sudden neurological deficits char by loss of motor
control, altered sensation, cognitive or language
impairment & disequilibrium or coma
 Causes & Risk Factors
 Accounts for 1 out of every 15 deaths
 The 3rd leading cause of death in most developed
countries
 The leading cause of disability in adults
 Caused by non-traumatic brain injury resulting from
occlusion or rupture of cerebral blood vessels
 Factors modifiable by lifestyle changes: cigarette
smoking, hypercholesterolemia, obesity, heart disease
 Non-modifiable risk factors: age, sex, race, previous
stroke
 Thrombotic Stroke
 Assoc with atherosclerotic plaque formation
occurring frequently at major branching sites
 Occurs often in the presence of chronic
hypertension
 SSx of transient monocular blindness or
amaurosis fugax are likely due to microemboli
from the internal carotid artery
 Embolic Stroke
 Majority of embolic strokes have a cardiac origin
 Atrial fibrillation: a significant risk factor for
embolic stroke as a result of poor arterial
mobility and outflow
 Other causes: mural thrombus within the LV after
MI
 Char by sudden neurologic deficit without
previous or progressive symptoms
 Hemorrhagic Stroke
 Intracerebral
 site of rupture: deep perforating cerebral arteries
 if px survives: rapid neurological recovery during the
1st 2 or 3 months after hemorrhage
 Subarachnoid
 bleeding that occurs within the dural space around
the brain
 most commonly caused by rupture of a saccular
aneurysm or an arteriovenous malformation
Transient Ischemic Attack (TIA)
 An event in which neurological symptoms develop and
disappear over several minutes & completely resolves
within 24 hours
 Reversible Ischemic Neurological Deficit (RIND):
transient neurological event that lasts longer than 24
hours; results from small infarctions of the deep
subcortical gray & white matter, resulting in only
temporary impairment
 Stroke in Evolution: an unstable ischemic event char by
progressive development of more severe neurological
impairment & is often assoc with active occlusive
thrombosis of a major cerebral artery
 Completed Stroke: a stable neurological status is reached
 Clinical Stroke Syndromes
 Internal Carotid Artery Stroke  Middle Cerebral Artery Stroke
 most common site of  contra hemiplegia/hemianesthesia
atherosclerosis & thrombosis  dysphagia
leading to TIA & stroke  uninhibited neurogenic bladder
 most severe at proximal 2 cm of  upper division: Broca aphasia
ICA
 lower division: Wernicke’s
aphasia
 Posterior Cerebral Artery
Stroke
 hemisensory deficit
 Anterior Cerebral Artery
Stroke
 visual impairment  contralateral hemiplegia; LE>UE
 visual agnosia  contralateral hemianesthesia
 prosopagnosia  akinetic mutism (abulia)
 alexia without agraphia
 memory deficits
 Stroke Related Impairments
 motor incoordination & balance problems
 spasticity
 sensory disturbances
 neglect syndromes
 dysphagia
 bladder & bowel incontinence
 apraxia: disorders of skilled movement; usually seen in L
hemisphere strokes
 dressing apraxia
 constructional apraxia
 language & communication disorders
 aprosody: lack of rhythmic pattern & vocal intonation of
speech; pxs speak at an even tempo with flat intonation
 alexia: an inability to comprehend the meaning of
written or printed words and sentences
 agraphia: inability to write properly
 aphasia: impairment of language
Broca aphasia: a type of aphasia in which there is
a deficit in speech production or language output,
often accompanied by a deficit in communicating by
writing, signs, etc. Syn: anterior aphasia, ataxic
aphasia, motor aphasia, expressive aphasia, nonfluent
aphasia.
Wernicke aphasia: aphasia in which there is
impairment in the comprehension of spoken and
written words, associated with effortless, articulated,
but paraphrastic, speech. Syn: fluent aphasia,
impressive aphasia, posterior aphasia, psychosensory
aphasia, receptive aphasia, sensory aphasia.
 Diagnosis & Tests
 Head CT or head MRI -- determine if the stroke was caused by
bleeding (hemorrhage) or other lesions, to define the location
&extent of the stroke.
 ECG (electrocardiogram) -- used to diagnose underlying heart
disorders.
 Echocardiogram -- used if the cause may be an embolus (blood clot)
from the heart.
 Carotid duplex (a type of ultrasound) -- used if the cause may be
carotid artery stenosis (narrowing of the major blood vessels
supplying blood to the brain).
 Heart monitor -- to determine heart arrhythmia
 Cerebral (head) angiography – to identify the blood vessel
responsible for the stroke, used if surgery is being considered.
 Blood work may be done to exclude immune conditions or abnormal
clotting of the blood that can lead to clot formation.
 Treatment
 Thrombolytic medicine, like tPA, breaks up blood
clots and can restore blood flow to the damaged area
 Analgesics (pain killers) may be needed to control
severe headache.
 Anti-hypertensive medication may be needed to
control high blood pressure
 For hemorrhagic stroke, surgery is often required to
remove pooled blood from the brain and to repair
damaged blood vessels
 Complications
 Problems due to loss of mobility (joint contractures, pressure
sores)
 Permanent loss of movement or sensation of a part of the body
 Bone fractures
 Muscle spasticity
 Permanent loss of brain functions
 Reduced communication or social interaction
 Reduced ability to function or care for self
 Decreased life span
 Side effects of medications
 Aspiration
 Malnutrition
 TRAUMATIC
BRAIN INJURY
 Types of Injury
 Open Injury
• an injury of direct penetration th/ the skull to the brain
• ex: gunshot wound, knife/sharp object penetration, direct trauma
 Closed Injury
• an injury to the brain w/o penetration th/ the skull
• ex: concussion, hematoma, hypoxia, drug overdose, drowning, acc/deceleration
injuries
 Primary Injury
• initial injury to the brain sustained by impact
• ex: skull penetration, skull fractures
• coup lesion: a direct lesion of the brain under the point of impact
• contrecoup lesion: injury on the other side of the brain due to rebound effect of the
brain after impact
 Secondary Injury
• occurs as a response to the initial injury
• ex: hematoma, hypoxia, ischemia, posttraumatic epilepsy
 Secondary Injury :
Occur as a Response to the Initial injury;

Depressed Hematoma or
 Level of Consciousness
 Coma: a state of unconsciousness & a level of
unresponsiveness to all stimuli
 Stupor: a state of general unresponsiveness with arousal
occurring from repeated stimuli
 Obtundity: a state of consciousness that is characterized by a
state of sleep, reduced alertness to arousal, & delayed
responses to stimuli
 Delirium: char by disorientation, confusion, agitation, &
loudness
 Clouding of consciousness: char by quiet behavior, confusion,
poor attention, & delayed responses
 Consciousness: a state of alertness, awareness, orientation &
memory
 Memory Impairments
 Anterograde Amnesia
• the inability to create new memory
• is usually the last to recover after a comatose state
• contributing factors: poor attention, distractibility, & impaired
perception of stimuli
 Posttraumatic Amnesia
• the time between the injury & when the patient is able to recall
recent events
• px does not recall the injury or events up until this point of
recovery
• used as an indicator of the extent of damage
 Retrograde Amnesia
• inability to remember events prior to the injury
• may progressively decrease with recovery
 Acute Diagnostic Management
 Glasgow coma scale: level of arousal & cortex
function
 CAT scan/MRI: intracranial structures
 X-ray: fractures
 Cerebral angiography
 EEG: localizing structural damage
 Radioisotope imaging: allows for two
dimensional concentrated view of the brain
 Glasgow Coma Scale
 A neurological assessment tool used initially
after injury to determine arousal & cerebral
cortex function
 A total score of 8 or less correlates to coma in
90% of patients
 Scores of 9 to 12 indicate moderate brain
injuries
 Scores from 13 to 15 indicate mild brain
injuries
 Elements of the scale
 The scale comprises three tests: eye, verbal
and motor responses. The three values
separately as well as their sum are considered.
The lowest possible GCS (the sum) is 3 (deep
coma or death), whilst the highest is 15 (fully
awake person).
 Best eye response (E)
There are 4 grades:
 Eyes opening spontaneously.
 Eye opening to speech. (Do not confuse with
an awaking of a sleeping person; if so, score 4,
not 3.)
 Eye opening to pain. (Put pressure on the
patient’s fingernail bed; if no response then try
supraorbital and sternal pressure/rub.)
 No eye opening.
 Best verbal response (V)
There are 5 grades:
 Oriented. (Patient responds coherently and
appropriately to questions such as the patient’s name
and age, where they are and why, the year, month, etc.)
 Confused. (The patient responds to questions
coherently but there is some disorientation and
confusion.)
 Inappropriate words. (Random or exclamatory
articulated speech, but no conversational exchange).
 Incomprehensible sounds. (Moaning but no words.)
 None.
 Best motor response (M)
There are 6 grades:
 Obeys commands. (The patient does simple things as
asked.)
 Localizes to pain. (Purposeful movements towards
changing painful stimuli; e.g.. hand crosses mid-line
and gets above clavicle when supra-orbital pressure
applied.)
 Withdraws from pain (pulls part of body away when
pinched; normal flexion).
 Flexion to pain (decorticate response).
 Extension to pain (decerebrate response, adduction,
internal rotation of shoulder, pronation of forearm).
 No motor response.
 Interpretation
 Individual elements as well as the sum of the
score are important. Hence, the score is
expressed in the form "GCS 9 = E2 V4 M3 at
07:35".
 Generally, comas are classified as:
 Severe, with GCS ≤ 8
 Moderate, GCS 9 - 12
 Minor, GCS ≥ 13.
 Rancho Los Amigos Levels of
Cognitive Functioning
I. No response
• px appears to be in a deep sleep
• completely unresponsive to any stimuli
II. Generalized response
• reacts inconsistently & non-purposefully to stimuli in a
nonspecific manner
III. Localized response
• reacts specifically but inconsistently to stimuli
IV. Confused-agitated
• bizarre, non-purposeful behavior
• uncooperative, (-) person/object discrimination
V. Confused-inappropriate
• able to respond to simple commands fairly consistently but
responses become non-purposeful/random with complex
commands
VI. Confused-appropriate
• shows goal-directed behavior but dependent on external
input or direction
VII. Automatic-appropriate
• appears appropriate & oriented but frequently robot-like
• shows minimal to no confusion
VIII. Purposeful-appropriate
• able to recall & integrate past/recent events
• shows new learning, needs no supervision
 Guidelines for Treatment
 Emphasis on motivation; focus on orientation
 promote independence
 Education in compensatory strategies for
success
 Use of calm voice & simple commands
 Family education & support can enhance &
assist in the rehabilitation process
SPINAL CORD
INJURY
 Alternate Names:
 Spinal cord compression, Spinal cord trauma
Definition
 Spinal cord injury is damage to the spinal cord that results
from direct injury to the cord itself, or from indirect injury
from damage to the bones, soft tissues, and blood vessels
surrounding the spinal cord.
 Spinal cord injuries occur in approximately 12,000 to 15,000
people per year in the U.S. About 10,000 of these people are
permanently paralyzed, and many of the rest die as a result of
their injuries. Most spinal cord trauma occurs to young,
healthy individuals. Males between 15 and 35 years old are
most commonly affected.
 Only about 5% of spinal cord injuries occur in children. The
fatality rate is higher with pediatric spine injuries.
 Pathophysiology
 Due to indirect forces produced by movement
of the head & trunk, and less often from
indirect injury to a vertebra
 Common mechanism in SCI: flexion,
compression, hyperextension, and flexion-
rotation; these forces may result in either a
fracture and/or dislocation
 The intensity and combination of forces affects:
 the type and location of fracture
 the amount of dislocation
 the extent of soft tissue damage
● WHIPLASH:Not a precise Term but refers to Injury to the Cervical Vertebrae
WHIPLASH:
& adjacent Soft Tissues produced by sudden Jerking either backward or forward
acceleration of the Head in relation to Vertebral Col. (Maybe from Car Accident?
PROBABLE CAUSE OF WHIPLASH INJURY
 Causes & Risk Factors
 Motor vehicles accidents
 Falls
 Sports injuries
 Gunshot wounds
 Rheumatoid arthritis
 Osteoporosis
 Cuts
 Bleeding, fluid accumulation, and swelling can occur
inside the spinal cord or outside the spinal cord (but
within the spinal canal)
 Risk factors include participating in risky physical
activities, not wearing protective gear during work or
play, or diving into shallow water.
 Direct injury, such as cuts, can occur to the spinal
cord, particularly if the bones or the discs have been
damaged. Fragments of bone (from fractured
vertebrae, for example) or fragments of metal (such as
from a traffic accident) can cut or damage the spinal
cord. Direct damage can also occur if the spinal cord
is pulled, pressed sideways, or compressed. This may
occur if the head, neck, or back are twisted
abnormally during an accident or injury.

The accumulation of blood or fluid can compress the

spinal cord and damage it.
 Ascending Tracts
 Lateral & Anterior
Spinothalamic Tracts
 pain & temperature sensation
and crude touch
 Dorsal Column
 fine touch, proprioception,
two-point discrimination
 Dorsal & Ventral
Spinocerebellar Tracts
 proprioceptive and
exteroceptive stimuli for
movement and position sense
 Spinoreticular Tract
 deep and chronic pain
 Descending Tracts
 Anterior Corticospinal
(Direct Pyramidal Tract)
 Pathway for control of
voluntary motion
 Lateral Corticospinal
(Crossed Pyramidal
Tract)
 Pathway for control of
voluntary motion
 Vestibulospinal Tract
 For postural reflexes
 Rubrospinal Tract
 Serves as motor junction
 Reticulospinal Tract
 For modulation of sensory transmission esp. pain;
spinal reflexes
 Tectospinal Tract
 For reflex head turning
 Medial Longitudinal Fissure
 For coordination of head and eye movements
 Quadriplegia
 refers to partial or complete paralysis of all four
extremities & trunk, including respiratory muscles and
results from lesions of the cervical cord
Paraplegia
 refers to partial or complete paralysis of all part of the
trunk and both lower extremities, resulting from lesions
of the thoracic or lumbar spinal cord or sacral roots
Complete Lesions
 no sensory or motor function below the level of the
lesion.
 caused by a complete transection, severe compression,
or extensive vascular impairment of the cord
 Incomplete Lesions
 characterized by preservation of some sensory or
motor function below the level of injury.
 often results to contusion produced by pressure on the
cord from displaced bone and/or soft tissue or from
swelling within the spinal canal.
 may also result from transection of the cord
Brown-Sequard Syndrome
 occur from hemisection of the spinal cord and is
typically caused by stab wounds
 partial lesions occur more frequently; true
hemisection are rare
 asymmetrical clinical features
 ipsilateral paralysis; contralateral hemiparesis
 Anterior Cord Syndrome
 frequently related to flexion injuries of the cervical
region with resultant damage to the anterior portion
of the cord and/or its vascular supply from the
anterior spinal artery
 complete motor paralysis & sensory deficits below
the level of the lesion except the dorsal column
pathways or proprioceptive sensation
Central Cord Syndrome
 the most common incomplete cord syndrome
 most commonly occurs from hyperextension injuries
to the cervical region
 more severe neurologic involvement of the UE than
the LE; (+) bladder dysfunction
 C5 to C6: most frequent site of injury
 assoc with congenital/degenerative narrowing of the
spinal canal
Posterior Cord Syndrome
 it is an extremely rare syndrome resulting in deficits of
function served by the posterior columns
 clinical picture include:
 preservation of motor function, sense of pain, and
light touch
 loss of proprioception and epicritic sensations below
the level of lesion
Sacral sparing
 refers to an incomplete lesion on which the most
centrally located tracts are spared.
 varying levels of innervation from sacral segments
remain intact.
 clinical signs include perianal sensation, rectal
sphincter contraction, cutaneous sensation in the
“saddle areas”, and active contraction of the sacrally
innervated toe flexors
Cauda Equina lesions
 cauda equina: the collection of lumbosacral nerve
roots & fibers that are bundled together below the
termination of the cord at L2
 flaccid, areflexic paralysis
 (+) bladder/bowel paralysis
 Signs & Symptoms
When spinal cord injuries occur near the neck, varying degrees
of symptoms can affect both the arms and the legs:
 weakness, paralysis
 breathing difficulties (from paralysis of the breathing muscles)
 spasticity (increased muscle tone)
 sensory changes
 numbness
 pain
 loss of normal bowel and bladder control
 constipation
 incontinence
 bladder spasms
 When spinal injuries occur at chest level, varying degrees of
symptoms can affect the legs:
 weakness, paralysis
 breathing difficulties (from paralysis of the breathing muscles)
 spasticity (increased muscle tone)
 sensory changes
 numbness
 pain
 loss of normal bowel and bladder control
 constipation
 incontinence
 bladder spasms

Injuries to the cervical or high thoracic cord may also result in:
 abnormal blood pressure
 blood pressure fluctuates quickly and through a wide range
 can be worsened with pain or bladder spasms
 abnormal sweating; trouble maintaining proper temperature
 Diagnosis & Tests
 A neurologic examination indicates the location of the injury,
if it is not immediately evident.
 The reflexes may be abnormal or may be absent in affected
areas of the body.
 Muscle spasticity is common as a late effect of spinal cord
injury.

 Spine X-rays may show fracture or damage to the bones of the

spine.
 A CT scan or MRI of the spine may pinpoint the location and
extent of spinal cord trauma and demonstrate any compressive
lesions like blood clots (hematomas).
 Rarely a myelogram (an X-ray of the spine after injection of
dye) may be necessary.
 Somatosensory evoked potential (SSEP) testing or magnetic
stimulation may determine if signals can get through the spinal
cord.
 SCI Level Determinants
C4 Neck flexors, scalenes, diaphragm
C5 Deltoid, biceps; biceps reflex
C6 Wrist extensors, brachioradialis reflex
C7 Triceps, wrist flexors; triceps reflex
C8 Interossei, finger flexors
T1Interossei
T6Accessory muscles of respiration & upper back extensors;
upper abdominal reflex
T12 Thoracic, abdominal and back muscles; lower abdominal reflex
L1Hip flexors
L2Knee extensors (quadriceps)
L3Hip adductors
L4Ankle dorsiflexors (tibialis anterior); patellar reflex
L5Long toe extensors (EHL)
S1 Peroneus longus & brevis; ankle reflex
 The extent of sensory and motor
loss resulting from a spinal cord
injury depends on the level of
the injury because nerves at
different levels control sensation
and movement in different parts
of the body.
 The distribution is as follows:
C1-C4: head and neck; C3-C5:
diaphragm; C5-T1: shoulders,
arms, and hands;T2-T12: chest
and abdomen (excluding internal
organs); L1-L4: abdomen
(excluding internal organs),
buttocks, genitals, upper legs;
L4-S3: legs; S2-S4: genitals,
muscles of the perineum.
 Treatment
 Corticosteroids, such as dexamethasone or
methylprednisolone:
 to reduce swelling that may damage the spinal cord. If spinal
cord compression is caused by a mass (such as a hematoma
or bony fragment)
 should begin as soon as possible after the injury.

 Surgery:
 to remove fluid or tissue that presses on the spinal cord
(decompression laminectomy).
 to remove bone fragments, disc fragments, or foreign objects
or to stabilize fractured vertebrae (by fusion of the bones or
insertion of hardware).

 Bedrest may be needed to allow the bones of the spine,

which bears most of the weight of the body, to heal.
 Anatomic realignment is important.
 Spinal traction may reduce dislocation and/or may
be used to immobilize the spine.
 The skull may be immobilized with tongs (metal
braces placed in the skull and attached to traction
weights or to a harness on the body).
 Rehabilitation
 Extensive physical therapy, occupational therapy,
and other rehabilitation interventions
 Assists the person in coping with disability that
results from spinal cord trauma.
 Prognosis
 Death is possible, particularly if there is paralysis of
the breathing muscles.

 The level of injury affects the outcome.

 Injuries near the top of the spine result in more
extensive disability (numbness and paralysis,
breathing difficulty) than injuries low in the spine.
 Recovery of some movement or sensation within one
week usually indicates eventual recovery of most
function, although this may take six months or more.
 Losses that remain after six months are more likely to
be permanent.
 Complications
 paralysis (paraplegia,  increased risk of injury to
quadriplegia) numb areas of the body
 loss of sensation  pain
 loss of bladder control  complications of immobility:
 increased risk of urinary  deep vein thrombosis
tract infections  pulmonary infections
 increased risk of chronic  skin breakdown
bilateral obstructive  contractures
nephropathy  shock
 loss of bowel control  extreme blood pressure
 loss of sexual functioning fluctuations
(male impotence)  spasticity (late complication)
 paralysis of breathing
muscles
SEIZURES
 Convulsions
 Convulsions are when a person's body shakes rapidly
and uncontrollably. During convulsions, the person's
muscles contract and relax repeatedly.
 The term "convulsion" is often used interchangeably
with "seizure," although there are many types of
seizure, some of which have subtle or mild symptoms
instead of convulsions. Seizures of all types are
caused by disorganized and sudden electrical activity
in the brain.
 Causes
 alcohol use; barbiturates,  meningitis
intoxication or withdrawal  poisoning
 brain illness or injury  stroke
 choking  toxemia of pregnancy
 electric shock  uremia related to kidney
 fever (particularly in young failure
children)  venomous bites and stings
 head injury  withdrawal from
 heart disease benzodiazepines (such as
 heat intolerance Valium)
 malignant hypertension  low blood sugar
 Signs & Symptoms
 Brief blackout followed by period of confusion
 Sudden falling
 Drooling or frothing at the mouth
 Grunting and snorting
 Breathing stops temporarily
 Uncontrollable muscle spasms with twitching and jerking
limbs
 Loss of bladder or bowel control
 Eye movements
 Teeth clenching
 Unusual behavior like sudden anger or laughter or picking at
one's clothing
 Assessment & Intervention
 When a seizure occurs, the main goal is to protect the
person from injury.
 Cushion the person's head.
 Loosen tight clothing, especially around the person's
neck.
 Turn the person on his or her side. If vomiting occurs, this
helps make sure that the vomit is not inhaled into the
lungs.
 Look for a medical I.D. bracelet with seizure instructions.
 Stay with the person until recovery or until you have
professional medical help. Meanwhile, monitor the
person's vital signs (pulse, rate of breathing).
 Do Not
 DO NOT restrain the person.
 DO NOT place anything between the person's teeth
during a seizure (including your fingers).
 DO NOT move the person unless he or she is in
danger or near something hazardous.
 DO NOT try to make the person stop convulsing. He
or she has no control over the seizure and is not
aware of what is happening at the time.
 DO NOT give the person anything by mouth until the
convulsions have stopped and the person is fully
awake and alert.
 Emergency Assistance
 for first time seizures
 seizures more than 2 to 5 minutes in duration
 the person does not awaken or have normal behavior
after a seizure
 the person had a seizure in water
 the person is pregnant, injured, or has diabetes
 the person does not have a medical ID bracelet
(instructions explaining what to do)
 there is anything different about this seizure
compared to the person's usual seizures
 Seizures
 aka convulsions
 are paroxysmal, sensory, or cognitive manifestations
of spontaneous, abnormally synchronous discharges
of collection of neurons in the cerebral cortex
 SSx can include strange sensations and perceptions
(e.g. hallucinations), unusual or repetitive muscle
movements, autonomic visceral activity, and the
onset of a confusional state or loss of consciousness
 the most common disorder encountered in pediatric
neurology
 Simple Partial Seizures
 aka elementary partial  flushing, tachycardia, diaphoresis,
seizures, partial seizures with hypo/hypertension
elementary symptoms, focal  prodrome (aura): a sensory
seizures warning sign of impending
 SSx depend on the area of seizure activity
the brain where neuronal  may progress to complex partial
discharge is taking place seizures or generalized tonic-
clonic seizures resulting in
 Jacksonian seizure:
unconsciousness
sequential involvement of
body parts in an epileptic-
type march
 sensory SSx: tingling &
crawling sensation
 Complex Partial Seizures
 involved impairment of consciousness
 often arise from the temporal lobe
 referred to as temporal lobe seizures or psychomotor seizures
 automatisms: repetitive, non-purposeful activity e.g. lip
smacking, grimacing, patting, or rubbing clothing
 hallucinations: déjà vu, jamais vu
 overwhelming fear, uncontrolled forced thinking or a flood of
ideas, feeling of detachment and depersonalization
 Generalized-Onset Seizures
 the most common type in young children
 SSx: unconsciousness, varying bilateral
degrees of symmetric motor responses
 divided into:
 absence seizures
 atonic seizures
 myoclonic seizures
 major motor seizures
 Absence Seizures
 generalized, non-convulsive epileptic events
 expressed mainly as disturbances in consciousness
 referred to as petit mal seizures
 typical absence seizures: blank stare, motionless, &
unresponsiveness & motions (lip smacking, mild eyelid clonic
motion, increased postural tone)
 atypical absence seizures: similar except for greater alterations
in muscle tone and less abrupt onset and cessation
 Atonic Seizures
 char by a sudden, split-second loss of muscle
tone leading to slackening of the jaw, drooping
of the limbs, or falling to the ground
 aka drop attacks
 Myoclonic Seizures
 involve brief involuntary muscle contractions
induced by stimuli of cerebral origin
 bilateral jerking of muscles, generalized or
confined to the face, trunk or one or more
extremities
 tonic seizures: char by a rigid, violent
contraction of the muscles, fixing the limbs in
a strained position
 Tonic-Clonic Seizures
 formerly called grand mal seizures
 the most common major motor seizure
 vague warning
 experiences a sharp tonic contraction of the muscles
with extension of extremities and immediate loss of
consciousness
 (+) incontinence, cyanosis
 tonic phase followed by a clonic phase, involving
rhythmic bilateral contraction and relaxation of the
extremities
 Treatment
 Anticonvulsant therapy
 the most effective and widely used treatment for
the symptoms of epilepsy
 considered effective if the patient is free of seizures
for at least one year
 can produce a variety of side effects, including
nausea, fatigue, dizziness, and weight change, and
can also increase the risk of birth defects
 ineffective for more than one third of known cases
of epilepsy; more than 30% of patients with
epilepsy cannot maintain adequate control of their
seizures.
 Surgery
 Recommended for some patients for whom medication
cannot effectively control the frequency or severity of their
seizures
 A treatment option only in extreme cases where doctors
can identify the specific site in the brain where seizures
originate
 The most promising candidates for surgery are those with a
single lesion on the temporal, frontal, or occipital lobes of
the brain
 Prior to surgery, the patient must complete extensive
testing to determine the precise patterns of seizures and to
locate their point of origin in the brain using the EEG
 The anterior temporal lobe and hippocampus are the most
common areas in which tissue is removed
 More than 83% of patients become free of seizures
following surgery. Ninety-seven percent show significant
improvement in their condition
 Vagus Nerve Stimulation
 A form of treatment for some cases of epilepsy
that are unresponsive (referred to as refractory
epilepsy) to other forms of medical therapy
 Also be recommended for patients who cannot
tolerate the side effects of medication
 Involves implanting a device that stimulates the
Vagus nerve, located in the left side of the neck.
 In one study, this treatment reduced seizures by
78%
 Ketogenic Diet
 A treatment option for patients who are not good candidates
for surgery or who have had little success with
anticonvulsant medication
 Most appropriate for young children whose parents can
follow the rigid requirements of the diet. Older children and
adults tend to have greater difficulty in sticking to the dietary
rules for an extended period of time
 a stringent diet that is very high in fat, but low in proteins,
carbohydrates, and calories. The excessive fat produces high
levels of a substance called ketones (which the body makes
when it breaks down fat for energy). Somehow these ketones
help reduce the incidence of epileptic seizures.
 The success of this form of treatment varies. For some
patients, the high fat diet is the best form of treatment. For
others, the diet is less effective.
ALTERATIONS
IN MOBILITY

Eric B. Panopio, M.D.

FRACTURES
 Fractures
 a break in the structural continuity of bone which
may arise from a single traumatic incident, repetitive
stress or abnormal weakening of bone
 Open fracture: one in which the laceration in the
skin or mucous membranes communicates with the
fracture hematoma
 Closed fracture: those in which the overlying skin
covering is intact
 Compound fracture: if the broken bone punctures
the skin
Fracture Types
 Oblique - a fracture which
goes at an angle to the axis
 Comminuted - a fracture of
many relatively small
fragments
 Spiral - a fracture which
runs around the axis of the
bone
 Compound - a fracture (also
called open) which breaks
the skin
Fracture Types
 Greenstick - an
incomplete fracture in
which the bone bends
 Transverse - a fracture
that goes across the
bone's axis
 Simple - a fracture
which does not break
the skin
Fractures
Fractures of the bones are
classified in a number of
ways.
 A simple fracture involves a
single fracture line through
a bone.
 A comminuted fracture is
one in which the bone has
been fractured into two or
more fragments.
 An open fracture is one in
which the fractured bone
penetrates the skin
 Causes
The following are common causes of broken
bones:
 Fall from a height
 Motor vehicle accidents
 Direct blow
 Child abuse
 Repetitive forces, such as those caused by
running, can cause stress fractures of the foot,
ankle, tibia, or hip
 Signs & Symptoms
 A visibly out-of-place or misshapen limb or joint
 Swelling
 Intense pain
 Bruising
 Numbness and tingling
 Bleeding
 Broken skin with bone protruding
 Limitation or unwillingness to move a limb
 Prevention
 Wear protective gear while skiing, biking, roller blading, and
participating in contact sports
 Create a safe home for young children. Gate stairways and keep
windows closed.
 Teach children how to be safe and look out for themselves.
 Supervise children carefully. There is no substitute for
supervision, no matter how safe the environment or situation
appears to be.
 Prevent falls by not standing on chairs, counter tops, or other
unstable objects. Remove throw rugs and electrical cords from
floor surfaces. Use handrails on staircases and non-skid mats in
bathtubs. These steps are especially important for the elderly.
 Assessment & Intervention
 Keep the person still and calm.
 Examine the person closely for other injuries.
 If the skin is broken, it should be treated immediately to prevent
infection. Don't breathe on the wound or probe it. If possible, lightly
rinse the wound to remove visible dirt or other contamination, but
do not vigorously scrub or flush the wound. Cover with sterile
dressings.
 Immobilize the broken bone with a splint or sling in the position you
found it. Possible splints include a rolled up newspaper or strips of
wood. Immobilize the area both above and below the injured bone.
 Apply ice packs to reduce pain and swelling.
 Take steps to prevent shock. Lay the person flat, elevate the feet
about 12 inches above the head, and cover the person with a coat or
blanket. However, DO NOT move the person if a head, neck, or
back injury is suspected.
 Do Not
 DO NOT move the person unless the broken bone is firmly
secured with a splint or sling.
 DO NOT move a person with an injured hip, pelvis, or upper
leg unless it is absolutely necessary. If you must move the
person, pull the person to safety by his clothes (such as by the
shoulders of a shirt, a belt, or pant-legs).
 DO NOT move a person who has a possible spine injury.
 DO NOT attempt to straighten a bone or change its position
unless blood circulation appears hampered.
 DO NOT try to reposition a suspected spine injury.
 DO NOT test a bone's ability to move.
 DO NOT give the person anything by mouth.
External Fixation Device
 An external fixation device
may be used to keep
fractured bones stabilized
and in alignment.
 The device can be adjusted
externally to ensure the
bones remain in an optimal
position during the healing
process.
 This device is commonly
used in children and when
the skin over the fracture
has been damaged.
Internal Fixation Device
 An internal fixation
device may be used to
keep fractured bones
stabilized and in
alignment. The device is
inserted surgically to
ensure the bones remain
in an optimal position
during and after the
healing process.
Treatment
 Casting
 Open reduction, and internal
fixation- this involves a surgery to
repair the fracture-frequently,
metal rods, screws or plates are
used to repair the bone, and
remain in place, under the skin,
after the surgery.
 Open reduction, and external
fixation- this involves a surgery to
repair the fracture, and placement
of a external fixation device on
the limb with the fracture. This
device is an external frame which
supports the bone and hold it in
the correct position while it is
healing.
 Bone Fracture Repair
 While the patient is pain-free (general or local anesthesia), an incision is made
over the fractured bone. The bone is placed in proper position and screws,
pins, or plates are attached to or in the bone temporarily or permanently. Any
disrupted blood vessels are tied off or burned (cauterized). If examination of
the fracture shows that a quantity of bone has been lost as a result of the
fracture, especially if there is a gap between the broken bone ends, the surgeon
may decide that a bone graft is essential to avoid delayed healing.
 If bone grafting is not necessary, the fracture can be repaired by the following
methods:
a) one or more screws inserted across the break to hold it.
b) a steel plate held by screws drilled into the bone.
c) a long fluted metal pin with holes in it, is driven down the shaft of the bone
from one end, with screws then passed through the bone and through a hole in
the pin.
 In some cases, after this stabilization, the microsurgical repair of blood vessels
and nerves is necessary. The skin incision is then closed in the usual fashion.
Aftercare
 The advantage of internal fixation
is that it often allows early
mobility and faster healing.
Unless the internal fixation causes
problems, it is not necessary or
desirable to remove it. The long-
term prognosis is excellent. The
length of the hospital stay
depends on factors such as the
condition of the bone, the
presence of infection, the state of
the blood and nerve supply, and
presence of other injuries.
Children's bones heal rapidly,
usually in 6 weeks time
 Terminology
of Fracture

● Bennett’s Fracture:
➮ Intra-articular Fracture of
the Base of the First
Metacarpal Bone ;

● Smith’s or Reverse Barton’s

Fracture:
➮ Fracture of Distal
Radius w/ Palmar
or Anterior
displacement;
Palmar Side
 Terminology
of Fracture
● Colle’s Fracture:
➮ Fracture of the distal
Radius w/ Dorsal or
Posterior displacement;

● Galleazi’s Fracture:
➮ Single Lone Fracture
of the distal 3rd of
the Radius associated

w/ Radio-Ulnar Joint
dislocation;
 Terminology
of Fracture

● Monteggia’s Fracture:
➮ Fracture of the Shaft
of Ulna with;
➮ Dislocation of the
Head
of the Radius.

● Hangman’s Fracture:
➮ Fracture of the
C2 Pedicle;
 Terminology
of Fracture

● Jefferson’s Fracture:
➮ C1 Fracture 2ndary
to Axial Bone load
on top of the Head;

● Stress or March Fracture:

➮ Foot Fracture 2ndary to
marching or persistent
walking involving the
Second Metatarsal and
Calcaneus Bone;
 Terminology of
Fracture
● Greenstick Fracture:
➮ Incomplete Fracture in
w/c the Angulating Force
bends the cortex on the
compression side & breaks
on the distraction site.

Non-Dislocation of
the Radial Head
● Nightstick Fracture:
➮ Fracture of the Shaft of
the Ulna w/out dislocation
of the Radial Head.
 Bennett’s fracture: intraarticular fracture of the base of the first
metacarpal
 Smith’s or Reverse Barton’s fracture: fracture of distal radius
with palmar or anterior displacement
 Colle’s fracture: fracture of the distal radius with dorsal or
posterior displacement
 Galleazi’s fracture: single lone fracture of the radius in distal third
associated with radio-ulnar joint dislocation
 Monteggia’s fracture: fracture shaft of ulna with dislocation of the
radial head
 Hangman’s fracture: fracture through the pedicle of C2
 Jefferson’s fracture: C1 fracture secondary to axial load on top of
the head
 Stress or March fracture: foot fracture secondary to marching or
persistent walking; usually involves the 2nd metatarsal & calcaneus
 Nightstick fracture: fracture of the shaft of the ulna without
dislocation of the radial head
 Greenstick fracture: have incomplete fracture in which angulating
force bends the cortex on the compression side & breaks on the
distraction site
1st cervical vertebra called atlas
Has no body
Holds up the head
Movement between atlas &
occipatal bone is responsible for the
“YES” motion

2nd cervical vertebra called the axis

Vertebra responsible for shaking
the head “NO”
This rotation occurs around a
process called the dens
ARTHRITIC
CONDITIONS
Eric B. Panopio, M.D.
 JUVENILE
RHEUMATOID
ARTHRITIS
 Alternate Names:
 Still’s disease
Definition
 Chronic arthritis beginning in childhood, most
cases of which are pauciarticular, i.e., affecting
few joints.
 A chronic, inflammatory disease resulting in
joint pain and inflammation.
 It may result in joint damage. It usually occurs
before age 16.
JUVENILE RHEUMATOID ARTHRITIS
 3 Categories of JRA
Systemic JRA:
 10%; involves joint pain and swelling as well
as fevers and rash; unknown cause
Polyarticular JRA:
 40%; multiple painful, swollen joints;
unknown cause; may evolve to RA
Pauciarticular JRA:
 50%; few joints involved; (+) HLA-B27 are
at increased risk for this arthritis.
 There are 3 major types of juvenile rheumatoid arthritis:

CHRACTERISTIC : POLYARTICULAR PAUCIARTICULAR SYSTEMIC

ONSET

Number of joints Five or more Four or less Any #

involved:

Joints affected : Usually small joints of Usually large joints, such Any joint
fingers and hands as knees, ankle or elbow
Also possibly weight Usually particular joint on
bearing joints one side of body
Often same joint on both
sides of the body.

Gender Boys and girls

More girls than boys More girls than boys equally
affected :
Body temp: Low grade fever Low grade fever High spiking fever
lasting for weeks
or months
 Signs & Symptoms
Arthritis symptoms:
 joint stiffness on arising in the morning
 limited range of motion
 slow rate of growth or uneven arm or leg growth
 hot, swollen, painful joints
 a child my stop using an affected limb
 back pain
Systemic JRA symptoms:
 Fever, usually high fevers every day
 Rash that comes and goes with the fever
 Swollen lymph nodes (glands)
JRA can also cause eye inflammation. These symptoms include:
 red eyes
 eye pain
 photophobia (increased pain when looking at a light)
 visual changes
 Diagnosis & Tests
 PE: shows swollen, warm, and tender joints
that hurt to move, the child may have a rash,
enlarged liver & spleen, & lymphadenopathies
 Blood tests may include:
 CBC
 ESR (sedimentation rate)
 ANA
 RA factor
 HLA antigens for HLA B27
 Treatment
The goal is to preserve mobility and joint function and
support the patient and family through a long chronic
illness.

Therapeutic medications include:

 Non-steroidal anti-inflammatory agents (NSAIDS)
 Corticosteroids

 Physical therapy and exercise programs may be

recommended. Surgical procedures may be indicated,
including joint replacement.
 Prognosis
 JRA is seldom life-threatening. Long periods
of spontaneous remission are typical.
 Approximately 75% of JRA patients
eventually enter remission with minimal
functional loss and deformity.
 Complications
 total joint destruction of the major weight-
bearing joints
 decrease in or loss of vision
 chronic spondyloarthropathy (back stiffness)
 LEGG-CALVE-
PERTHES DISEASE
 Alternate Names:
 Coxa Plana
Definition
 Epiphysial aseptic necrosis of the upper end of
the femur.
 An idiopathic form of osteonecrosis of the
femoral head occurring in children which
results in some flattening of the head of the
femur
 Causes & Risk Factors
 occurs in children between 3 and 12 y/o
 more common in boys
 affected children are usually slightly shorter in stature
 cause of ischemia of the femoral head: ↑ intraarticular
pressure as a result of disease or trauma
 necrosis of bone & marrow of the epiphysis of the
femoral head takes place & is followed by slow
resorption of the dead bone
 Signs & Symptoms
 Most constant early sign: limp associated with muscular
spasm
 LOM on all hip motions especially IR & abduction
 Atrophy of thigh, hip & leg muscles
 Knee pain (may be the only symptom, initially)
 Persistent thigh or groin pain
 Leg length discrepancy
 Hip stiffness restricting movement in the hip
 Difficulty walking, walking with a limp (which is often
painless)
 Limited range of motion
 Diagnosis & Tests
 (+) Crescent sign: x-ray of the subchondral
bone may appear as a thin radioluscent line
just beneath the joint surface
 LOM on all hip motions especially IR &
abduction
LEGG-CALVE-PERTHES DISEASE
Normal Femoral Head
w/in the Acetabulum
 Treatment
 Most important factor in preventing hip deformity:
containment of femoral head within the concave hemisphere
of the acetabulum by maintaining the hip in a position of
abduction & mild IR using brace
 Surgery: usually reserved for hips with a poor prognosis e.g.
patients older than 6 yrs at onset, who have sustained total or
nearly total involvement of femoral head.
 The aim of treatment is to protect the bone and joint from
further stress and injury while the healing process takes place.
 Bed rest or crutches: may be needed during the initial phase.
 Brace, cast, or splint: used to immobilize the hip's position
while bone regrowth takes place.
 Prognosis
 The outcome is usually good with treatment.
Most bone will heal with minimal lasting
deformity.
 Complications
 Osteoarthritis
RICKETS
 Alternate Names:
 Juvenile osteomalacia, Infantile Osteomalacia,
Rachitis, Osteomalacia in Children, Renal Rickets,
Vitamin D Deficiency

Definition
 A disease of children in which the bones fail to
calcify.
 Bones soften & a definite bowing of the weight-
bearing bones of the legs occurs.
 Due to lack of calcium in the diet or lack of vitamin
D
 Causes & Risk Factors
 Nutritional causes of rickets occur because of a lack
of vitamin D in the diet or in association with
malabsorption disorders characterized by poor fat
absorption.
 A dietary lack of calcium and phosphorous (rather
than a lack of vitamin D) may also play a part in the
nutritional causes of rickets. Rickets caused by a
dietary lack of these minerals is rare in developed
countries because calcium and phosphorous are
present in milk and green vegetables.
 Signs & Symptoms
 Bone pain or tenderness  Increased tendency toward bone
 Arms fractures
 Legs  Dental deformities
 Spine  Delayed formation of teeth
 Pelvis  Defects in the structure of teeth,
 Skeletal deformities holes in the enamel
 Bowlegs
 Increased incidence of cavities in
the teeth (dental caries)
 Forward projection of the
breastbone (pigeon chest)
 Progressive weakness
 "Bumps" in the rib cage (rachitic
 Decreased muscle tone (loss of
rosary) muscle strength)
 Asymmetrical or odd-shaped  Muscle cramps
skull  Impaired growth
 Spine deformities (spine curves  Short stature (adults less than 5
abnormally, including scoliosis feet tall)
or kyphosis)
 Pelvic deformities
RICKETS
 Prevention
 Ensure adequate intake of calcium, phosphorus, and
vitamin D. This may require dietary supplements in
people who have gastrointestinal or other disorders.
 Renal (kidney) causes of vitamin D malabsorption
should be treated promptly.
 Levels of calcium and phosphorus should be monitored
regularly in people who have renal disorders.
 Genetic counseling may help people with a family
history of inherited disorders that can cause rickets.
 Diagnosis & Tests
 Calcium levels may be low.
 Tetany (prolonged muscle spasm) may occur if serum
levels of calcium are low.
 Chvostek's sign may be positive (a spasm of facial muscles
occurs when the facial nerve is tapped) indicating low
serum levels of calcium.
 Serum calcium will confirm calcium levels.
 Serum phosphorus may be low.
 Serum alkaline phosphatase may be high.

Other tests and procedures include the following:

 PTH
 Urine calcium
 Calcium (ionized)
 Treatment
 The treatment goals are to relieve symptoms and
correct the cause of the condition. The underlying
cause must be treated to prevent recurrence.
 The replacement of deficient calcium, phosphorus, or
vitamin D.
 Positioning or bracing may be used to reduce or
prevent deformities.
 Some skeletal deformities may require corrective
surgery.
 Prognosis
 If rickets is not corrected while children are
still growing, skeletal deformities and short
stature may be permanent.
 If it is corrected while the child is young,
skeletal deformities often diminish or
disappear with time.
 Complications
 Chronic skeletal pain
 Skeletal deformities
 Skeletal fractures, may occur without cause
RHEUMATOID
ARTHRITIS
 Alternate Names:
 Arthritis deformans, Nodose rheumatism, RA
Definition
 A systemic rheumatic disease which primarily
affects the synovial lining of diarthrodial joints
 Causes & Risk Factors
 Autoimmune etiology
 Pannus formation: destructive component
causing deformities
 Women 2-3X more affected
 Peak incidence in women: between the 4th &
6th decades
 Signs & Symptoms
 Fatigue  radial deviation of wrist
 General discomfort or malaise  ulnar deviation of fingers
 Loss of appetite  swan neck deformity due to intrinsic
 Low-grade fever tightness with hyperextensible PIP jts
 Joint pain/swelling/stiffness
 boutonniere deformity
 Often symmetrical
 cocked toe deformity
 Limited range of motion American Rheumatism Association
Revised Criteria
 Morning stiffness > 1 hour 1. morning stiffness
 Deformities of hands and feet 2. soft tissue swelling – 3 or more areas
 Round, painless nodules under the 3. swelling/arthritis of PIP, MCP or
skin wrist
 Skin redness or inflammation 4. symmetric swelling arthritis
 Paleness 5. rheumatoid nodules over bony
 Swollen glands prominence
 Eye burning, itching, and discharge 6. (+) serum rheumatoid factor
 Numbness and/or tingling 7. periarticular osteopenia in hand/wrist
ADULT RHEUMATOID ARTHRITIS
ADULT RHEUMATOID ARTHRITIS
Internal Joint Findings

1.
Gross Characteristic Findings in Late Stage RA
ADULT RHEUMATOID ARTHRITIS
 Rheumatoid arthritis is an
autoimmune disease in
which the body's immune
system attacks itself.
 The pattern of joints
affected is usually
symmetrical, involves the
hands and other joints and is
worse in the morning.
 Rheumatoid arthritis is also
a systemic disease,
involving other body
organs, whereas
osteoarthritis is limited to
the joints.
 Over time, both forms of
arthritis can be crippling.
 Prevention
 Rheumatoid arthritis has no known prevention.

 It may be possible to prevent further damage

of the joints with proper early treatment.
 Diagnosis & Tests
 Joint x-rays
 Rheumatoid factor test is positive in about
75% of people with symptoms
 Erythrocyte sedimentation rate is elevated
 CBC may show low hematocrit (anemia) or
abnormal platelet counts
 Goals of Treatment
 Pain relief  Increase strength & endurance
 moist heat: 15 minutes BID  isometric exercise:
 splinting for wrist and hand treadmill/cycle, ergometer &
water exercise
 Prevention & correction of
 moderation
deformities  suppress inflammation thoroughly
 protective splints before exercising
 joint mobilization
 exercise done under careful,
controlled conditions with
 molded shoe insoles & extra monitoring of exercise joints
depth shoes to provide support
and spread pressure
 joint preservation & work
 Psychological counseling
simplification technique  job history and modification
 Complications

 joint destruction  anemia

 gastrointestinal bleeding  low or high platelets
 heart failure  eye disease
 pericarditis  cervical (neck) spine
 pleuritis instability
 lung disease  neuropathy
 vasculitis.
GOUT
 Definition
 an attack of a metabolic disease marked by
uric acid deposits in the joints. The disorder
causes painful arthritis, especially in the joints
of the feet and legs.
 Causes & Risk Factors
 Hyperuricemia may be due to an excess rate of
uric acid production & a decrease in the renal
excretion of uric acid
 Epidemiology:
 Peak at 5th decade among adult men
 Peak among women, usually postmenopausal
 Stages of Gout
1. Asymptomatic Hyperuricemia
 defined as BUA > 8.1 mg/dL in men, 7.2 mg/dL in women
2. Acute Intermittent Gout
 usually occurs decades after initial hyperuricemia
 onset: warmth, erythema, swelling & extreme pain in affected joint
 may be accompanied by fever & chills
 90%: occurs in the first MTP
3. Intercritical Stage
 completely asymptomatic patient but monosodium urate crystals
can still be seen in joints
4. Chronic Tophaceous Gout
 develops 10 or more years after acute intermittent attack
 joints swollen & uncomfortable but with less pain
 tophi: develops with uric acid > 11 mg/dL; found in fingers, wrist,
ears, knees & ulnar aspect of forearm
 Signs & Symptoms
 Joint pain  The joint may be warm and red
 Begins suddenly  Fever may be present
 Affects one or more joints  Skin lump which may drain
(hip pain, knee pain, ankle chalky material
pain, foot pain, shoulder pain,
elbow pain, wrist pain, hand  Clinical Associations of Gout:
pain, or pain in other joints)
 renal disease
 The great toe, knee, or ankle
 hypertension
joints are most often affected
 hyperlipidemia
 Joint swelling of the affected
joints
 Stiffness of the joint
TOPHI IN GOUT
 GOUT

As If Your Foot
Is Eaten By the
DEVIL !

TOPHUS
 Prevention
 The disorder itself may not be preventable
 Avoidance of precipitating factors: trauma,
alcohol consumption, and dietary purines.
 Diagnosis & Tests
A physical examination of the joints shows
acute arthritis.
 Synovial fluid analysis shows uric acid
crystals.
 Uric acid (blood test) may be elevated.
 Joint X-rays may be normal.
 Treatment
 To reduce the symptoms of acute attacks, colchicine,
NSAID’s, or corticosteroids are often prescribed
 In chronic gout, long term medical supervision and
Rx are indicated. Low-purine diet & avoidance of
excessive alcohol may help to prevent attacks
 Tophaceous deposits can be prevented or reversed by
prolonged use of xanthine oxidase inhibitor,
allopurinol, which reduces the formation of uric acid
 In late cases, large tophi may require surgery
 Complications
 Side effects of medications
 Chronic gouty arthritis
 Kidney stones
 Kidney dysfunction
OSTEOARTHRITIS
 Alternate Names:
 Degenerative Joint Disease, DJD, Hypertrophic
Osteoarthritis, OA, Osteoarthrosis
Definition
 Osteoarthritis is a chronic disease causing
deterioration of the joint cartilage (the softer parts of
bones, which cushion their connections to each other)
and the formation of new bone (bone spurs or
osteophytes) at the margins of the joints.
 Most common disease of both axial and peripheral
diarthrodial joints
 Osteoarthritis is a chronic
disease of the joint cartilage
and bone, often thought to
result from "wear and tear"
on a joint, although there are
other causes such as
congenital defects, trauma
and metabolic disorders.
Joints appear larger, are stiff
and painful and usually feel
worse the more they are
used throughout the day.
 Variant Forms of OA
 Primary Generalized OA
 reveals involvement of the DIPs and PIPs of the hands, the 1 st CMC
joint, knees, hips & MTP joints
 Erosive Inflammatory OA
 involves primarily the DIPs or PIPs of the hands
 there is eventual development of deformity & ankylosis
 Ankylosing Hyperostosis
 a.k.a. diffuse idiopathic skeletal hyperostosis (DISH)
 characterized by flowing ossification along the anterolateral aspect
of the vertebral bodies
 Secondary OA
 produces clinical findings similar to those seen in the primary form
of the disease
Narrowing of Joint Spaces due to
Progressive Loss of Joint Cartilages
 KNEE JOINT in OA
Your Observation: 1) Formation of Osteophytes (Spurs) along Joint Margins;
2) Erosion of Cartilage & Meniscus exposing the Bone;
Osteoarthritis of the HIP JOINT
 Osteoarthritis is
associated with the aging
process and can affect
any joint. The cartilage
of the affected joint is
gradually worn down,
eventually causing bone
to rub against bone.
Bony spurs develop on
the unprotected bones
causing pain and
inflammation.
 Signs & Symptoms
 gradual and subtle onset of deep  It may first appear without
aching joint pain symptoms between 30 and 40
 worse after exercise or weight years of age and is present in
bearing almost everyone by the age of 70.
 often relieved by rest Symptoms generally appear in
middle age. Before the age of 55
 joint swelling it occurs equally in both sexes.
 limited movement However, after 55 the incidence is
 morning stiffness higher in women.
 grating of the joint with motion
 joint pain in rainy weather  Involvement of the lumbar spine
is seen most commonly at the L3
 Heberden’s nodes: formation of to L4 area
spurs at dorsolateral 7 medial
aspects of the DIP joint
 Bouchard’s nodes: nodal
osteoarthritis at the PIP joint
 Prevention
 Weight reduction in women reduces the risk of
developing knee osteoarthritis.
 Diagnosis & Tests
 Physical exam can show limited range of
motion, grating of a joint with motion, joint
swelling, and tenderness.
 X-ray shows osteophytes & joint space
narrowing
 Synovial fluid analysis showing non-
inflammatory features
 Osteoarthritis

Assessment & Diagnostic Work-Up:

♚ P.E. Reveals:
☞ Tender & Enlarge Inflamed Joints;
♚ Radiologic Findings:
☞ Characterized by Progressive Loss of Joint
Cartilage represented by ________________________;
Narrowing of Joint Spaces;
☞ There are formation of __________________
Osteophytes (Spurs) along
Joint Margins & on the Subchondral Bone as
cartilage tends to regenerate;
♚ Serum Studies NOT Useful in the Dx of this Disorder;
 Treatment
Principles of Treatment Non-pharmacologic
 symptom relief  physical therapy modalities
 maintaining or improving  weight reduction program
function  assistive devices
 limiting physical disability
 avoiding drug toxicity Surgical
 involves joint replacement
Pharmacologic procedures for severe cases
 acetaminophen of DJD
 NSAID’s
 intra-articular steroids
 Complications
 decreased ability to walk or perform activities
of daily living (personal hygiene, house
chores, cooking, etc.)
 complications from treatments including
adverse reactions to drugs or surgical
complications
 VISUAL &
AUDITORY
ALTERATIONS
Eric B. Panopio, M.D.
ALTERATIONS
IN VISION
Eye
 The eye is the organ of sight, a nearly spherical
hollow globe filled with fluids (humors).
 The outer layer or tunic (sclera, or white, and cornea)
is fibrous and protective.
 The middle tunic layer (choroid, ciliary body and the
iris) is vascular. The innermost layer (the retina) is
nervous or sensory.
 The fluids in the eye are divided by the lens into the
vitreous humor (behind the lens) and the aqueous
humor (in front of the lens).
 The lens itself is flexible and suspended by ligaments
which allow it to change shape to focus light on the
retina, which is composed of sensory neurons.
 The Eye and Vision

 Eye has three layers

 Sclera
 Outermost layer

 Known as “White of the eye”

 Extends over front of eye as transparent cornea

Eye Illustrated
 Uvea
 Uvea
 Middle, vascular layer
 Consists of:
 Choroid
 Ciliary body
 Muscle controls shape of lens
 Allows for accommodation
 Iris
 Muscular ring
 Controls size of pupil
 Determines eye color
 Retina
 Innermost layer
 Actual visual receptor
 Consists of specialized cells:
 Rods
 Function in dim light
 Low visual acuity

 Do not respond to color

 Cones
 Active in bright light
 High visual acuity

 Respond to color
 Vision
 Requires refraction
 Focuses on specific point on retina
 Energy transmitted to brain via optic nerve

 Optic disk
 Connection point for optic nerve to retina
 Fovea
 Point of greatest visual acuity
 Surrounded by macula
 Eye Protection
 Orbit = bony socket
 Eyelids
 Conjunctiva
 Thin membrane
 Covers anterior portion of eye

 Eyebrows
 Eyelashes
 Tears
 Lacrimal glands
 Bathe eyes with lubricating fluid
 Fluid drains into nose
Congenital
Cataracts
A Congenital Cataract involves clouding of the
Lens of the Eye that is present at birth.
CONGENITAL CATARACT
 Causes & Risk Factors
Causes of congenital cataracts include the following:
 Galactosemia
 Chondrodysplasia syndrome
 Congenital rubella syndrome
 Down syndrome (trisomy 21)

Rubella are more frequent cause of congenital cataract

than syphilis
 Signs & Symptoms
 Opacity of the lens, often evident at birth
without special viewing equipment and
appearing as a whitish discoloration in an
otherwise normally dark pupil
 Failure of an infant to show visual awareness
of the world around him or her (if present in
both eyes)
 Nystagmus (unusual rapid eye movements)
 Diagnosis & Tests
 Ophthalmologist: complete eye examination
 Pediatrician: blood tests & x-rays
 Treatment
 The treatment involves surgical cataract
removal followed by placement of an
intraocular lens (IOL).
 Treatment for any underlying disorder may be
needed.
Strabismus
 Alternate Names:
 Squint, Cast, Phoria, Cross-eye (Esotropia), Wall-eye (Exotropia)
Definition
 Strabismus is a manifest lack of parallelism of the visual axes of the
eyes
 Strabismus involves deviation of the alignment of one eye in
relation to the other.
 Strabismus is caused by a lack of coordination between the eyes.

Paralytic strabismus:
 due to weakness or paralysis of 1 or more of the extraocular
muscles.
Nonparalytic strabismus:
 more common & are due to underlying ocular or visual defects such
as may occur in cataracts, lesions of the optic nerve or macula, high
refractive errors or asymmetric refractive errors
 Cross-Eyed or Esotropia
Give the Defect: Deviation of the Eye to the Medial Side or
towards the Nose;
 Wall-Eyed or Exotropia

Give the Defect: Deviation of the Eye to the Lateral Side

Extrinsic Muscle of the Right Eye
Cross-Eyed or Esotropia
 Causes & Risk Factors
 In most cases of strabismus in children, the cause is unknown.
In more than half of these cases, the problem is present at or
shortly after birth (congenital strabismus).

Some other disorders associated with strabismus in children

include:
 Retinopathy of prematurity
 Retinoblastoma
 Traumatic brain injury
 Hemangioma near eye during infancy
 Trisomy 18
 Congenital rubella
 Cerebral palsy
 Signs & Symptoms
 Eyes that appear crossed
 Eyes that do not align in the same direction
 Uncoordinated eye movements
 Double vision
 Vision in only one eye with loss of depth
perception
 Diagnosis & Tests
 The physical examination will include a
detailed examination of the eyes.
Tests include:
 Standard ophthalmic exam
 Treatment
 Strategies to strengthen the weakened muscles and
thereby realign them.
 Glasses may be prescribed.
 Eye muscle exercises may be prescribed.
 If amblyopia is present, patching of the preferred eye
may be done to force the child to use the amblyopic
eye.
 Surgery may be required to realign the eye muscles if
strengthening techniques are unsuccessful.
Retinoblastoma
 Alternate Names:
 Cancer - Retina, Tumor - Retina
Definition
 Retinoblastoma is a malignant ocular
neoplasm of childhood
 In familial forms, the disease is commonly
bilateral and multiple within an eye; in
sporadic cases, rarely so.
 Retinoblastoma is a malignant tumor (cancer)
of the retina (part of the eye) that generally
affects children under the age of 6.
Retinoblastoma
Retinoblastoma
Retinoblastoma
 Signs & Symptoms
• Most frequent sign: leukocoria=white or “cat’s eye"
reflex in the pupil.
 A white glow in the eye that is often seen in
photographs taken with a flash; instead of the typical
"red eye" from the flash, the pupil may appear white
or distorted
 Pupil, white spots
 Crossed eyes
 A red, painful eye
 Poor vision
 The iris may be a different color in each eye.
 Diagnosis & Tests
 An examination of the eye with dilation of the
pupil
 A head CT scan: to evaluate tumor & spread
 A head & eye echoencephalogram: an
ultrasound of the eye
 Treatment
 Treatment options depend upon the size and
location of the tumor.
 Small tumors may be treated by laser surgery.
 Radiation and chemotherapy may be needed if
the tumor has spread beyond the eye.
 The eye may need to be removed if the tumor
does not respond to other treatments.
Glaucoma
 Definition
 Glaucoma is a disease of the eye characterized
by increased intraocular pressure and
excavation and atrophy of the optic nerve;
produces defects in the visual field and may
result in blindness.
 Glaucoma involves increased fluid pressure
inside the eye (intraocular pressure), which
damages the optic nerve and causes partial
vision loss and can progress to blindness.
 Normal Optic Disc as seen on Opthalmoscopic Exam
● Central Retinal Artery
Contents of the Optic Disc: ● Central Retinal Vein
● Optic Nerve
 Causes & Risk Factors
 Increased pressure occurs when the fluid within
the eye (called aqueous humor) does not drain
properly.
 The pressure pushes on the junction of the optic
nerve and the retina at the back of the eye.
 This reduces the blood supply to the optic
nerve, which carries visual information from
the eye to the brain.
 For chronic glaucoma, risk factors include the following:
 Age over 40
 Family history of glaucoma
 Diabetes
 Nearsightedness

The risk factors for acute glaucoma include the following:

 Older age
 Family history of acute glaucoma
 Farsightedness
 Use of systemic anticholinergic medications (such as atropine
or eye dilation drops) in a high-risk individual

Acute, congenital, and secondary glaucoma are much less

common than chronic glaucoma.
 Signs & Symptoms
ACUTE:  Blurred or foggy vision
 Severe eye & facial pain  Mild, chronic headaches
 Loss of vision  Seeing rainbow-colored
 Cloudy vision with halos halos around lights
appearing around lights CONGENITAL:
 Red eye  Tearing
 Fixed, nonreactive pupil  Sensitivity to light
 Nausea & vomiting  Redness of the eye
CHRONIC:  Corneal haziness
 Gradual loss of  Enlarged cornea
peripheral vision
 Diagnosis & Tests
A standard ophthalmic examination may include:
 Retinal examination
 Intraocular pressure measurement by tonometry
 Visual field measurement
 Visual acuity
 Refraction
 Pupillary reflex response
 Slit lamp examination
Slit lamp Examination
 Central and peripheral vision is tested by using visual field
tests. Changes may indicate eye diseases, such as glaucoma or
retinitis.
 Treatment
Medications:
 Beta-adrenergic blocking eye drops
 Epinephrine drops
 Xalatan (latanoprost): a topical medication that helps drain the
aqueous outflow from the eye and lower the intraocular pressure.
Surgery
 Iridotomy:
 creates a drainage hole in the iris to relieve the pressure
 may be used in patients who have had acute episodes in the past to
prevent recurrence
 Laser treatment of the fluid drainage area in the eye may be used to
treat open angle glaucoma.
 In severe cases that are not responsive to medical treatment, surgery
can be done to create new outflow channels.
Cataracts
 Alternate Names:
 Lens Opacity
Definition
 A cataract is a complete or partial opacity of the
ocular lens or a cloudy or opaque area in the lens of
the eye .
 Classified as: immature, mature, and hypermature.
 Immature cataract: A lens that has some remaining
clear areas
 Mature cataract: a lens that is completely opaque.
 Hypermature cataract: has a liquefied surface that
leaks through the capsule and may cause
inflammation of other structures in the eye.
 Cataract

Immature Cataract: Hypermature Cataract:

Hypermature Cataract: Mature Cataract:

Opacity of
the Lens
 Causes & Risk Factors
 Cataracts are accelerated by environmental factors, such as
smoking or exposure to other toxic substances, or they may
develop at any time after an eye injury.
 Metabolic diseases such as DM greatly increase the risk for
cataracts.
 Medications such as cortisone, can accelerate cataract
formation.
 Factors that may contribute to cataract development are low
serum calcium levels, diabetes, long-term use of corticosteroids,
and various inflammatory and metabolic disorders.
 Environmental causes include trauma, radiation exposure, and
excessive exposure to ultraviolet light (sunlight).
 Signs & Symptoms
 Cloudy, fuzzy, foggy, or filmy vision
 Loss of color intensity
 Frequent changes in eyeglass prescription
 Impaired vision at night, especially while driving,
caused by glare from bright lights
 Problems with glare from lamps or the sun
 Halos around lights
 Double vision in an individual eye
 Decreased contrast sensitivity
 Prevention
 The primary prevention involves controlling
associated diseases and avoiding exposure to
factors known to promote cataract formation.
 Wearing sunglasses outside during the day to
reduce UV light exposure
 Abstinence from smoking will decrease the
risk of cataracts.
 Diagnosis & Tests
 Standard ophthalmic exam, including slit lamp
examination
 Ultrasonography of the eye in preparation for
cataract surgery
 Treatment
LENS REMOVAL:
 There are 2 types of surgery that can be used to remove lenses
that have a cataract.
 Extracapsular surgery consists of surgically removing the
lens, but leaving the back half of the capsule (the outer
covering of the lens) intact.
 Intracapsular surgery involves surgically removing the entire
lens, including the capsule. Today this procedure is done very
rarely.

LENS REPLACEMENT:
 The artificial lens is a synthetic disc called an intraocular lens. It
is usually placed in the lens capsule inside the eye.
Intraocular lens implants
 Prognosis
 For most people, cataract surgery has a low
risk of complications.
 With implanted artificial lenses, most people
no longer need corrective lenses for distance
vision.
 Glasses are usually necessary for reading.
 Complications
 Vision may not improve after cataract surgery if
other eye diseases such as macular degeneration
are present.
 In infants, amblyopia and decreased visual
development may occur as a result of cataracts.
 Amblyopia: Poor vision caused by abnormal
development of visual areas of the brain in
response to abnormal visual stimulation during
early development
 ERRORS OF
REFRACTION
 Errors of Refraction
 Myopia = nearsightedness
 Eyeball too long
 Images form in front of retina
 Hyperopia = farsightedness
 Eyeball too short
 Images form behind retina
 Astigmatism = irregularity in curve of cornea or
lens
 Glasses can correct most of these impairments
Errors of Refraction Illustrated
Visual Acuity Test
Myopia
 Alternate Names:
 Nearsightedness, Shortsightedness
Definition
 Myopia is the optical condition in which only rays from
a finite distance from the eye focus on the retina.
 Myopia is an error of visual focusing that makes distant
objects appear blurred.
 A nearsighted person can easily read the Jaeger eye chart
(the chart for near reading), but finds the Snellen eye
chart (the chart for distance) difficult to read. This
blurred vision results when the visual image is focused
in front of the retina, rather than directly on it.
 Causes & Risk Factors
 It occurs when the physical length of the eye is
greater than the optical length. For this reason,
nearsightedness often develops in the rapidly growing
school-aged child or teenager, and progresses during
the growth years, requiring frequent changes in
glasses or contact lenses. It usually stops progressing
as growth is completed in the early twenties.
 Nearsightedness affects males and females equally,
and those with a family history of nearsightedness are
more likely to develop it.
 Signs & Symptoms
 Blurred vision or squinting when trying to
see distant objects. (Children often cannot
read the blackboard, but can easily read a
book.)
 Eyestrain.
 Headaches
 Prevention
 There is no way to prevent nearsightedness.
Reading and watching television do not cause
nearsightedness.
 The use of glasses or contact lenses does not
affect the normal progression of myopia in the
growth years -- they simply focus the light so
the nearsighted person can see distant objects
clearly.
 Diagnosis & Tests
A general eye examination, or standard ophthalmic
exam may include:
 Visual acuity, both at a distance (Snellen), and close up
(Jaeger)
 Refraction test, to determine the correct prescription for
glasses
 Test of color vision, to test for possible color blindness
 Tests of the muscles which move the eyes
 Slit-lamp exam of the structures at the front of the eyes
 Measurement of the pressure of fluid in the eyes
 Retinal examination
 Treatment
 Nearsightedness is easily compensated for by
the use of eyeglasses or contact lenses, which
shift the focus point to the retina.
 LASIK: an excimer laser used to reshape the
cornea.
Hyperopia
 Alternate Names:
 Farsightedness
Definition
 Hyperopia is the optical condition in which
only convergent rays can be brought to focus
on the retina.
 Hyperopia is difficulty seeing objects which
are nearby.
 Causes & Risk Factors
 Farsightedness is the result of the visual image being
focused behind the retina rather than directly on it. It
may be caused by the eyeball being too small or the
focusing power being too weak.
 Farsightedness is often present from birth, but
children can often tolerate moderate amounts without
difficulty and most outgrow the condition.
 As aging occurs, glasses or contact lenses may be
required to correct the vision. A family history of
farsightedness is a risk factor.
 Signs & Symptoms
 Blurred vision of close objects
 Eye strain
 Aching eyes
 Headache while reading
 Crossed eyes (strabismus) in children
 Diagnosis & Tests
 Visual acuity
 Refraction
 Glaucoma testing
 Eye movements
 Slit-lamp
 Retinal examination
 Treatment
 Farsightedness is easily corrected with glasses
or contact lenses.
 Surgical techniques are available for
correcting farsightedness and can be used for
those who do not wish to wear glasses or
contacts.
Astigmatism
 Alternate Names:
 Astigmia
Definition
 A lens or optical system having different refractivity
in different meridians.
 A condition of unequal curvatures along the different
meridians in one or more of the refractive surfaces
(cornea, anterior or posterior surface of the lens) of
the eye, in consequence of which the rays from a
luminous point are not focused at a single point on
the retina.
 Astigmatism is a condition in which the cornea of the
eye is asymmetrically curved, causing out-of-focus
vision.
 Causes & Risk Factors
 The cause of astigmatism is unknown.
 It is usually present from birth, and often
occurs together with nearsightedness or
farsightedness.
 A minor degree of astigmatism is considered
normal and does not require correction.
Astigmatism is very common.
 Signs & Symptoms

 Difficulty in seeing fine detail, either close-up

or from a distance.
 Diagnosis & Tests
 Astigmatism is easily diagnosed by a standard
ophthalmic exam with refraction test.
 Special tests are not usually required.
 Children or others who cannot respond to
questions can have their refractive error
measured by a test using reflected light called
retinoscopy.
 Treatment

 Glasses or hard contact lenses will correct

astigmatism.
 Soft contact lenses do not work as well.
 Prognosis

 Vision is usually normal with the correct

glasses or contact lenses.
 Complications
 There are complications associated with
contact lenses (including the risk of corneal
abrasion), which may develop if contact lenses
are used.
 Unequal astigmatism may cause amblyopia.
 Retinal
Detachment
 Definition
 Retinal detachment is a loss of apposition
between the sensory retina and the retinal
pigment epithelium.
 Retinal detachment is a separation of the light-
sensitive membrane in the back of the eye (the
retina) from its supporting layers.
Retinal Detachment
 Causes & Risk Factors
 Retinal detachment may be caused by trauma, the
aging process, severe diabetes, or an inflammatory
disorder, but it frequently occurs spontaneously.

 The risk factors are nearsightedness, a family history

of retinal detachment, uncontrolled diabetes and
trauma.
 Approximately 10,000 people per year are affected
by retinal detachments.
 Signs & Symptoms
 Bright flashes of light, especially in peripheral
vision
 Translucent specks of various shapes (floaters)
in the eye
 Blurred vision
 Shadow or blindness in a part of the visual
field of one eye
 Prevention
 Use protective eye wear to prevent eye trauma.
 Control your blood sugar carefully if you have
diabetes.
 Consult your eye care specialist at least yearly,
especially if you have risk factors for retinal
detachment.
 Diagnosis & Tests
Tests to determine the integrity of the retina may include:
 Direct and indirect ophthalmoscopy
 Visual acuity
 Refraction test
 Color defectiveness determination
 Pupillary reflex response
 Slit lamp examination
 Intraocular pressure determination
 Ultrasound of the eye
 Retinal photography
 Fluorescein angiography
 Electroretinogram (a record of the electrical currents in the retina
produced by visual stimuli)
 Treatment
 Laser surgery can be used to seal the tears or holes in the
retina, which generally precede detachment.

 Another technique, the application of intense cold with an ice

probe (known as cryopexy), leads to the formation of a scar
that holds the retina to the underlying layer. This technique is
used in combination with the injection of a gas bubble and the
maintenance of specific head positions to prevent the re-
accumulation fluid behind the retina.

Surgical reattachment involves indentation of the sclera to

relieve pressure on the retina, allowing it to re-attach.
ALTERATIONS
IN AUDITORY
FUNCTION
Ear Anatomy
 The ear consists of
external, middle, and
inner structures. The
eardrum and the three
tiny bones conduct
sound from the eardrum
to the cochlea.
The Ear Illustrated
 The Ear
 Used for both hearing and equilibrium
 Divided into three parts
 Outer ear
 Pinna (auricle)
 External auditory canal (meatus)

 Contains cerumen (earwax)

 Tympanic membrane (eardrum)

 Transmits sound waves to middle ear

 The Ear (con’t)
 Middle ear
 Houses three ossicles
 Malleus (hammer)

 Incus (anvil)

 Stapes (stirrup)

 Soundwaves are transmitted from footplate of stapes

 Eustachian tube
 Connects middle ear to nasopharynx

 Equalizes pressure between outer and middle ear

 The Ear (con’t)
 Inner ear
 Complex labyrinth shape
 Filled with fluid
 Contains cochlea
 Organ of Corti

 Vestibular apparatus
 Sense of equilibrium

 Semicircular canals

 Vestibulocochlear nerve
 Cochlear branch transmits hearing impulses

 Vestibular branch transmits equilibrium impulses

 Hearing Loss
 Sensorineural hearing loss
 Damage to eighth cranial nerve or central
auditory pathway
 Caused by
 Heredity
 Toxins
 Exposure to loud noises
 Aging process

 Treatment
 Cochlear implant
 Conductive Hearing Loss
 Results from:
 Blockage in sound transmission to inner ear
 Causes include:
 Obstruction
 Severe infection

 Fixation of middle ear ossicles

 Usually treated successfully

OTITIS EXTERNA
EXTERNAL OTITIS OR ACUTE OTITIS EXTERNA
General Consideration & Causes:

■ Inflammation w/ Infection of the External Ear;

■ Causes maybe: Water w/in the Ear Canal also called
“Swimmer’s Ear”
_________________ Organisms enters the
External Ear tissues  causing Infection;
■ Most Common Pathogens: Bacterial & Fungal;
■ Common Bacteria: Staph. Aureus & Pseudomonas Species;
■ Common Fungus: Aspergillus Specie;
■ Maybe triggered by Allergies from Hair Sprays & Dyes
causing Allergic Dermatitis affecting the External Ear.
 EXTERNAL OTITIS OR OTITIS EXTERNA

Sns & Sxs:

■ Ear Pain or Aural Tenderness from Swelling & Inflammation ;
■ Initial Discharges maybe Watery to Serosanguinous;
■ Fever, Cellulitis of the Skin, Lymphadenopathy;
■ Hearing Loss from Obstruction of the Ear Canal;
■ Otoscopic Exam: Ear Canal is Edematous & Erythematous;
■ Ear Discharges maybe: Foul Smelling Yellow to Green in
Color for untreated cases;
■ Fungus Infection: Hair-like Black Spores visible grossly;
Treatment:
■ Principles of Treatment Aimed at:
☞ Relieving Discomfort;
☞ Reduce Swelling causing the Pain;
☞ Eradicating Infection.
■ Analgesic / Anti-pyretic for Pain & Fever;
■ Anti-biotic Ear Drops.
OTITIS MEDIA
 Alternate Names:
 Chronic Ear Infection, Chronic Otitis Media, Ear
Infection - Chronic, Middle Ear Infection - Chronic
Definition
 inflammation of the middle ear, or tympanum.

 Otitis media is an inflammation and/or infection of the

middle ear.
 Acute otitis media (acute ear infection) occurs when
there is bacterial or viral infection of the fluid of the
middle ear, which causes production of fluid or pus.
 Chronic otitis media occurs when the eustachian tube
becomes blocked repeatedly due to allergies, multiple
infections, ear trauma, or swelling of the adenoids.
Otitis Media
 EAR DRUM

NORMAL INFLAMMED
SECRETORY OTITIS
MEDIA

more commonly
known as “glue ear”.
caused by blockage
of the eustachian
tube as a result of
allergies, swollen
adenoids or other
infections of the nose
& throat, that
dampens down the
conduction of sound
and reduces hearing
 ACUTE OTITIS
MEDIA

also known as
“ bacterial otitis media

acute infection of the

middle ear usually
started by an infection
in the URT
is the most frequent
diagnosis of children
in clinical practice
 CHRONIC OTITIS
MEDIA

is the result of a prolong

middle ear infection with
perforation of the
eardrum.
affects 20-40% of all
children under the age 6
 Causes & Risk Factors
 Chronic otitis media occurs when the eustachian tube
becomes blocked repeatedly
 The infection may spread into the mastoid bone
(mastoiditis), or pressure from fluid build-up may
rupture the eardrum or damage the bones of the
middle ear.
 Ear infections are more common in children because
their eustachian tubes are shorter, narrower, and more
horizontal than in adults.
 Chronic ear infections are much less common than
acute ear infections.
 Signs & Symptoms
 Ear pain or discomfort
 Usually mild
 May feel like pressure in the ear

 Pus-like drainage from the ear

 Deafness

Note: Symptoms may be continuous or

intermittent, and may occur in one or both ears.
 Diagnosis & Tests
 An examination of the ear may show dullness,
redness, air bubbles, or fluid behind the eardrum.
 The eardrum may show drainage or perforation (a
hole in the eardrum). The eardrum may bulge out or
retract inward.

 Mastoid X-rays or a CT scan of the head or mastoids

may show spreading of the infection beyond the
middle ear.
 Treatment
 Treatment is focused on relief of symptoms and cure of the
infection.

 Antibiotics: for bacterial infection; may be oral or ear drop if

with hole in eardrum
 Surgical adenoidectomy: necessary to allow the eustachian
tube to open.
 Myringotomy: a surgical opening may be made in the
eardrum to allow fluid to drain. This may or may not include
placement of drainage tubes in the ear.

 Keep the ears clean and dry to prevent reinfection, esp. in

myringotomy
 Complications
 Permanent damage to the ear with partial or complete deafness
 Mastoiditis
 Cholesteatoma: A mass of keratinized squamous cell
epithelium and cholesterol in the middle ear, usually resulting
from chronic otitis media, with squamous metaplasia or
extension of squamous epithelium inward to line an expanding
cystic cavity that may involve the mastoid and erode
surrounding bone.
 Epidural abscess
 Permanent hearing loss is rare, but the risk increases the more
infections a child has.
MASTOIDITIS
 Definition
 Mastoiditis is an infection of the mastoid bone of the
skull.
 inflammation of any part of the mastoid process.

 Mastoid air cells are open, air-containing spaces in

one of the skull bones
 Mastoiditis is an infection of the bony air cells in the
mastoid bone, located just behind the ear. It is rarely
seen today because of the use of antibiotics to treat
ear infections. This child has noticeable swelling and
redness behind his right ear because of mastoiditis.
Normal Anatomy
 Causes & Risk Factors
 Mastoiditis is usually a consequence of a
middle ear infection (acute otitis media). The
infection may spread from the ear to the
mastoid bone of the skull.
 Mastoiditis most commonly affects children.
 Signs & Symptoms
 Ear pain or discomfort
 earache
 pain behind the ear

 Redness of the ear or behind the ear

 Fever, may be high or spike (have sudden high
increases)
 Headache
 Drainage from the ear
Normal Anatomy
Give Your Diagnosis: MASTOIDITIS
Acute Coalescent Mastoiditis w/
Subperiosteal Abscess
 Prevention
 Prompt and complete treatment of ear
infections reduces the risk of developing
mastoiditis.
 Diagnosis & Tests
 An examination of the head may indicate
mastoiditis.
 A skull X-ray or head CT scan or CT of the
ear may show an abnormality in the mastoid
bone.
 A culture of drainage from the ear may show
bacteria.
 Treatment
 Mastoiditis may be difficult to treat because it is
difficult for medications to reach deep enough into
the mastoid bone. It may require repeated or long-
term treatment. Antibiotics by injection, then
antibiotics by mouth are given to treat the infection.

 Surgery to remove part of the bone and drain the

mastoid (mastoidectomy) may be needed if antibiotic
therapy is not successful.
 Surgical drainage of the middle ear through the
eardrum (myringotomy) may be needed to treat the
underlying middle ear infection.
Mastoidectomy: Indications &
Procedure
 Complications
 Recurrence
 Partial or complete hearing loss of the affected
ear
 Destruction of the mastoid bone
 Spread of infection to the brain or throughout
the body
 Epidural abscess
OTOSCLEROSIS
 Definition
 A condition of the middle ear which mainly
affects the tiny stapes bone.
 Causes gradual hearing loss.
 Cause is not known
 Hereditary factors: family history of
otosclerosis
 Virus may trigger the disease.
 56 year old male who has
been deaf from 1947-1975.
He is currently hearing noise
in his left ear when he
stamps his feet, runs down
stairs, grunts or counts aloud.
The patient describes the
sensation as a strong
vibration that ends in a
fraction of a second.

Red arrows demonstrate

lucencies in the otic capsule
surrounding the structures of
the inner ear.

OTOSCLEROSIS
 Causes & Risk Factors
 Affects 1-2 in 100 people in the UK
 Ages 15-35, but sometimes develops in younger
children
 Women are affected twice as men
 Otosclerosis is the most frequent cause of middle ear
hearing loss in young adults
 Otosclerosis usually affects both ears, and is most
commonly seen in women, 15 to 30 years old.
Risks include pregnancy (which may trigger onset), a
Caucasian race and a family history of hearing loss.
 Signs & Symptoms
 Hearing loss
 Slow, progressive
 Hearing may be better in noisy environments than
quiet areas.
 Ringing in the ears (tinnitus)
 Diagnosis & Tests
An examination of the ears may rule out other
causes of hearing loss.

 An audiometry/audiology may determine the

extent of hearing loss.
 A head CT scan or head x-ray may be used to
distinguish otosclerosis from other causes of
hearing loss.
 Treatment
 Hearing aids
 Surgery (replacement of the stapes with artificial plastic bone)
 Fluoride tablet in drinking water
 Medications such as oral fluoride, calcium or vitamin D may help
to stabilize the hearing loss, but their benefit has not been proven.
 A hearing aid may be used to treat the hearing loss. This will not
cure or prevent the progression of the disease, but may help
alleviate the symptoms of hearing loss.
Surgery to remove the stapes and replace it with a prosthesis is
curative. This may be total replacement (stapedectomy) or a laser
may be used to make a hole in the stapes (stapedotomy) to allow
placement of the prosthesis.
MENIERE’S
DISEASE
 Alternate Names:
 Endolymphatic Hydrops, Hydrops
Definition
 Meniere's disease is a disorder of the inner ear
affecting balance and hearing, characterized
by abnormal sensation of movement (vertigo),
dizziness, loss of hearing in one or both ears,
and noises or ringing in the ear (tinnitus).
 Causes & Risk Factors
 The exact cause of Meniere's disease is unknown.
 In some cases, it may be related to middle ear
infection (otitis media), syphilis, or head injury.
 Other risk factors include recent viral illness,
respiratory infection, stress, fatigue, use of
prescription or nonprescription drugs including
aspirin, and a history of allergies, smoking, and
alcohol use. There may be genetic risk factors as well.
 Signs & Symptoms
 Abnormal sensation of movement of self or the environment
(vertigo)
 May be episodic
 Lasts from minutes to more than 8 hours
 Worse with sudden movement
 Dizziness
 Hearing loss in one ear
 Low frequency noises lost first
 Extent of hearing loss may change
 Noises or ringing in one ear (tinnitus)
 Nausea, vomiting
 Sweating (may be profuse)
 Uncontrollable eye movements
 Diagnosis & Tests
 A neurologic examination may show an
abnormality of cranial nerve VIII that may
include abnormalities of hearing, balance, or
eye movement.

Tests to distinguish Meniere's disease from

other causes of vertigo may include:
 Head CT scan or head MRI scan
 Treatment
 Treatment is focused on lowering the pressure
within the endolymphatic sac and on treating
symptoms, which tend to occur in discrete
"attacks."
 Complications
 Inability to walk or function due to
uncontrollable vertigo
 Hearing loss on the affected side
LARYNGITIS
 Definition
 Is an inflammation or swelling of the vocal
cords in response to an infection, irritation or
damage (trauma).
 Vocal cords become thicker and stiffer & do
not vibrate well.
 It can occur at any age from childhood to old
age.
Throat Anatomy
NORMAL LARYNX
LARYNGITIS
 Causes & Risk Factors
 Occurs during an upper respiratory infection
and is a self-limiting condition
 Several forms of laryngitis occur in children
and can lead to significant or fatal respiratory
obstruction such as epiglottitis
 Other causes of laryngitis include allergies and
trauma.
 Signs & Symptoms
 Recent or current upper respiratory infection
 Hoarseness
 Fever
 Swollen lymph nodes or glands in the neck
 Prevention
 Avoidance of upper respiratory infections
during cold and flu season may help.
 Using good hygienic practices
 Smoking cessation can help prevent
malignancies of the head and neck, and of the
lungs, which may lead to laryngitis.
 Diagnosis & Tests
 PE: hoarseness associated with a respiratory
tract infection
 Patients (particularly smokers) with persistent
hoarseness: for tests of the throat and upper
airway.
Treatment
 The voice should be rested
as much as possible.
 The body should be well
hydrated by drinking an
increased amount of water.
 Drinks containing caffeine
such as coffee, tea & cola &
irritants such as smoke
should be avoided.
 Throat lozenges can help
sooth and relax the throat.
 Simple over the counter
painkillers help with
discomfort.
 Treatment
 Since most common laryngitis is viral, treatment with
antibiotics is generally not indicated. Your health care
provider will make this decision.
 Voice rest helps both the voice and to reduce
inflammation of the vocal cords.
 A humidifier may provide comfort for the scratchy
feeling sometimes associated with laryngitis.
 Decongestants and pain killers may relieve symptoms
of an accompanying upper respiratory infection.
LARYNGEAL
CANCER
 Alternate Names:
 Cancer of the Glottis, Throat Cancer, Throat
Cancer, Vocal Cord Cancer
Definition
 Cancer of the throat involves malignant tumors
(growths) on the vocal cords, voice box
(larynx), or other areas of the throat.
 Causes & Risk Factors
 Smoking
 Excessive alcohol use

 Most cancers of the throat develop in adults

older than 50, and men are 10 times more
likely than women to develop throat cancers.
 Signs & Symptoms
 Hoarseness that does not resolve in 1 to 2 weeks
 Sore throat
 Neck pain
 Difficulty swallowing
 Swelling in the neck
 Weight loss
 Cough
 Coughing up blood
 Abnormal (high pitched) breathing sounds
 Prevention
 Minimize or avoid smoking and excess alcohol
use.
 Diagnosis & Tests
 An examination of the neck and throat may show
cancers of the throat. The sputum may appear bloody.
A lump may appear on the outside of the neck.
 Laryngoscopy: allows the physician to look into the
mouth and down the throat to see the tumor.

 Neck or cranial CT scan or cranial MRI: may show

throat cancer and help determine if the cancer has
spread to lymph nodes in the neck.
 Biopsy
 Treatment
 Treatment is aimed at destruction of the cancer and
prevention of spread of the cancer to other parts of
the body.

 When the tumor is small, either surgery or radiation

therapy alone can be used to eliminate the tumor.
 When the tumor is larger or has spread to lymph
nodes in the neck, combination radiation and
chemotherapy is often used to preserve the voice box
and is successful in most cases
 Prognosis
 Throat cancers can be cured in 90% of patients
if detected early.
 If the cancer has spread to surrounding tissues
or lymph nodes in the neck 50-60% of patients
can be cured.
 If the cancer has spread (metastasized) to parts
of the body outside the head and neck, the
cancer is not curable and treatment is aimed at
prolonging quality of life.
 Complications
 Airway obstruction
 Loss of voice and speaking ability
 Disfigurement of the neck or face
 Hardening of the skin of the neck
 Difficulty swallowing
 Spread of the cancer to other body areas
(metastasis)
 End:
Perception & Coordination
Alterations

Prepared by:
Eric B. Panopio, M.D.