Test 4 Flashcards
The brain consists of the ______, _____ & ______
cerebrum, brainstem, and cerebellum
The ____ is composed of the right and left hemispheres
cerebrum
Both hemispheres can be further divided into four major lobes.
Frontal
Temporal
Parietal
Occipital
The ______ lobe controls higher cognitive function, memory retention, voluntary eye movements, voluntary motor movement, and expressive speech in Broca’s area.
frontal
The _____ lobe contains integration of somatic, visual, and auditory data, and Wernicke’s area, which is responsible for receptive speech.
temporal
The _____ lobe is composed of the sensory cortex, controlling and interpreting spatial information
parietal
Processing of sight take place in the _____ lobe.
occipital
The basal ganglia, thalamus, hypothalamus, and limbic system are also located in the ______
cerebrum
The ______ includes the midbrain, pons, and medulla. The vital centres concerned with respiratory, vasomotor, and cardiac function are located in the medulla. The brainstem also contains the centres for sneezing, coughing, hiccupping, gagging, vomiting, sucking, and swallowing
brainstem
Located in the ______ is the reticular formation, which relays sensory information, influences excitatory and inhibitory control of spinal motor neurons, and controls vasomotor and respiratory activity
brainstem
a clear, colourless fluid similar to blood plasma and interstitial fluid. Circulates within the subarachnoid space that surrounds the brain, brainstem, and spinal cord. This fluid provides cushioning for the brain and spinal cord, allows fluid shifts from the cranial cavity to the spinal cavity, and carries nutrients
Cerebro-spinal fluid (CSF)
Peripheral nervous system
Spinal nerves
Cranial nerves
Autonomic nervous system (ANS)
Structures & Functions of Nervous System
Meninges
Skull
Vertebral column
Protective Structures
Central nervous system
Loss of neurons; brain weight decreases; cerebral blood flow decreases; CSF and neurotransmitter release decreases
Peripheral nervous system
Decreased nerve conduction and coordinated neuromuscular activity; intellectual performance remains constant; decreased sensory changes
Age related considerations
Cerebrospinal fluid analysis
Lumbar puncture
Radiological studies
Cerebral angiography
Computed tomography (CT)
Magnetic resonance imaging (MRI)
Positron emission tomography (PET)
Diagnostic Studies of Nervous System
may be done for someone who has NPH, high fever, headache – to check for infection, meningeal irritation
Lumbar puncture
Electroencephalography (EEG)
Electromyography (EMG) and nerve conduction studies
Evoked potentials
Electrographic studies
Carotid duplex studies
Transcranial Doppler ultrasonography
Combined Doppler and ultrasound studies
These tests can determine if there is a nerve problem, muscle problem, demyelination of the nerves.
Vascular system – flow in carotid, not the same blood flow to brain if narrow
Electrographic, Doppler & Ultrasound Studies
Factors that influence _____:
BP
Cardiac function
Intraabdominal pressure
Intrathoracic pressure
Body position
Temperature
Blood gases – especially CO2
Intracranial Pressure (ICP)
Occurs at the initial time of an injury that results in:
displacement,
Bruising
Or damage of the three components.
Primary Injury
Occurs after the primary injury:
Hypoxia
Ischemia
Hypotension
Edema
Increased ICP
Secondary Injury
Total pressure exerted because of the combined total volume of the 3 components of the skull:
Brain Tissue
Blood
CSF
ICP
Above 20mmhg
Life threatening
Occurs with increased brain tissue
Occurs with increased cerebral blood volume
Increased CSF
Any increase can results in hypercapnia, cerebral acidosis, impaired autoregulation, systemic hypertension, cerebral edema.
Increased ICP
An accumulation of fluid in the extravascular spaces of brain tissue
Results in increased tissue volume and possibly increased ICP
Can be caused by lesions, head injuries, brain surgery, cerebral infections, vascular insults and toxic or metabolic encephalopathic conditions
Can be vasogenic, cytotoxic, and interstitial
Cerebral Edema
Change in LOC
Changes in vital signs
Ocular signs
Change in Motor function
Headache
Vomiting
Manifestations of Increased ICP
- _______ intracranial adaptive capacity (related to decreased cerebral perfusion or increased ICP)
- Risk for ineffective cerebral tissue perfusion as evidenced by brain injury, brain neoplasm, cerebral aneurysm
- Risk for disuse syndrome as evidenced by alteration in level of consciousness, mechanical immobility, paralysis
Decreased
Any trauma to the
Skull
Scalp
Brain
Head trauma includes an alteration in consciousness, no matter how brief.
Head Injury
The majority of deaths after a ______ occur immediately after the injury, either from the direct head trauma or from massive hemorrhage and shock.
head injury
Scalp lacerations
Skull fractures
Head trauma
Focal injury (laceration, contusion)
Types of Head Injury
The most minor type of head trauma
Scalp is highly vascular _ profuse bleeding
Major complication is infection
Scalp lacerations
Linear or depressed
Simple, comminuted, or compound
Closed or open
Location of the fracture alters the presentation of manifestations.
Facial paralysis
Battle’s sign
Bilateral periorbital ecchymosis (raccoon eyes)
Rhinorrhea or otorrhea indicates that a fracture has traversed the dura.
Leaking fluid should be tested to determine if the fluid is cerebrospinal fluid (CSF).
Skull fractures
Diffused or localized
Diffuse (Concussion)
A sudden transient mechanical head injury with disruption of neural activity and a change in level of consciousness (LOC)
Brief disruption in LOC
Amnesia
Headache
Short duration
Head trauma
2 weeks to 2 months
Persistent headache
Lethargy
Personality and behaviour changes
Shortened attention span, decreased short-term memory
Changes in intellectual ability
Post-concussion syndrome (head trauma)
Widespread axonal damage following mild, moderate, or severe traumatic brain injury (TBI)
decreased LOC
increased ICP
Decortication, decerebration
Global cerebral edema
Diffuse axonal injury (head trauma)
Lacerations
Contusion
Focal injuries
Involve actual tearing of the brain tissue
Often occur in association with depressed and open fractures and penetrating injuries
Intracerebral hemorrhage is generally associated with cerebral laceration.
Surgical repair of laceration is impossible.
Prognosis is poor with large intracerebral lacerations.
Lacerations (Focal Injury)
Bruising of brain tissue within a focal area that maintains the integrity of the pia mater and arachnoid layers
Coup-contrecoup injury
Prognosis is dependent on the amount of bleeding around the contusion site.
Contusion (Focal Injury)
Results from bleeding between the dura and the inner surface of the skull
Neurological emergency
Venous or arterial origin
Epidural hematoma (complication)
Classic signs
Initial period of unconsciousness
Brief lucid interval followed by decrease in LOC
Headache
Nausea, vomiting
Focal findings
Occurs from bleeding between the dura mater and the arachnoid layer of the meningeal covering of the brain
Usually results from injury to the brain substance and its parenchymal vessels
Usually venous in origin
Much slower to develop into a mass large enough to produce symptoms
May be caused by tearing of small cortical arteries
Epidural hematoma (complication)
Signs within 48 hours of the injury
Similar signs and symptoms to brain tissue compression in increased intracranial pressure (ICP), decreased LOC, and headache
Patient appears drowsy and confused, ranging to unconsciousness
Ipsilateral pupil dilates and becomes fixed
Acute subdural hematoma
Occurs within 2–14 days of the injury
After initial bleeding, a subdural hematoma may appear to enlarge over time.
Subacute subdural hematoma
Develops over weeks or months after a seemingly minor head injury
Peak incidence in 50s and 60s age groups
Chronic subdural hematoma
Occurs from bleeding within the brain tissue
Usually occurs within the frontal and temporal lobes
Size and location of hematoma determine patient outcome
Intraparenchymal Hematoma
Result of traumatic forces damaging the superficial vascular structures that exist in the subarachnoid space
May predispose the patient to cerebral vasospasm and diminished cerebral blood flow (CBF), increasing the risk of ischemic damage following brain injury
Traumatic Subarachnoid Hemorrhage
Treatment principles
Prevent secondary injury
Manage ICP
Timely diagnosis
Surgery if necessary
Craniotomy
Craniectomy
Cranioplasty
Burr-hole approach
Diagnostic Studies and Interprofessional Care
Nursing assessment
Glasgow Coma Scale score
Neurological status
Presence of CSF leak
Nursing Management
Prevent motor vehicle accidents.
Promote wearing of safety helmets and seat belts.
Health promotion - Nursing implementation
Maintain cerebral oxygenation and perfusion.
Prevent secondary cerebral ischemia.
Monitor for changes in neurological status.
Treatment of life-threatening conditions will initially take priority in nursing care.
Major focus of nursing care relates to increased ICP
Eye conditions
Hyperthermia
Raise the head of patients leaking CSF.
Acute intervention - Nursing implementation
Nutrition
Bowel and bladder management
Spasticity
Dysphagia
Deep venous thrombosis
Hydrocephalus
Post-traumatic seizure
Mental and emotional support
Ambulatory and home care - Nursing implementation
Maintain normal cerebral perfusion pressure
Achieve maximal cognitive, motor, and sensory function
Experience no infection or hyperthermia
Achieve pain control
Evaluation - Expected outcomes
Acute inflammation of meningeal tissue
Always arachnoid mater and cerebrospinal infection
Is a medical emergency.
Untreated, the mortality rate is near 100%.
Bacterial meningitis
Increased cerebrospinal fluid (CSF) production
Purulent secretions spread to other areas of the brain through CSF.
If the process extends into the parenchyma, or if concurrent encephalitis is present, cerebral edema and increased intracranial pressure (ICP) become problematic.
Bacterial meningitis
Fever
Severe headache
Nausea, vomiting
Nuchal rigidity
Positive Kernig’s sign
Positive Brudzinski’s sign
Photophobia
↓ Level of consciousness (LOC)
Signs of ↑ ICP
Coma Seizures
Headache
Vomiting
Irritability
Bacterial meningitis
Acute complication is ↑ ICP
Residual neurological dysfunction
The optic nerve (CN II) is compressed by increased ICP.
Ocular movements are affected with irritation to nerves III, IV, and VI.
Irritation of CN VIII causes tinnitus, vertigo, and deafness.
Hemiparesis, dysphagia, and hemianopsia may occur and resolve over time.
Acute cerebral edema
Noncommunicating hydrocephalus if CSF flow obstructed
Waterhouse–Friderichsen syndrome
Bacterial meningitis - Complications
Blood culture
Lumbar puncture and analysis of CSF
X-rays of skull
CT Scan
MRI
Bacterial meningitis - Diagnostics
a group of symptoms caused when the adrenal glands fail to function normally. This occurs as a result of bleeding into the glands. Meningococcemia is a life-threatening infection that occurs when the bacteria Neisseria meningitidis invades the blood stream. – whole vascular system can collapse within the brain
Waterhouse-Friderichsen syndrome (WFS)
Rapid Diagnosis based on history and physical exam
Antibiotic therapy instituted after collection of specimens
Interprofessional Care
Neurological evaluation
Vital signs
Assessment of fluid intake and output
Evaluation of the lungs and skin
Nursing Assessment
Inadequate intracranial adaptative capacity
Hyperthermia
Potential for inadequate cerebral tissue perfusion
Acute pain
Bacterial Meningitis: Nursing Diagnoses
Patient will
Have minimal disorientation
Lack evidence of agitation
Have satisfactory pain relief
Participate in treatment
Have normal body temperature
Bacterial Meningitis: Evaluation
Most common causes are enterovirus, arbovirus, HIV, and herpes simplex virus (HSV)
Usually presents as a headache, fever, photophobia, and stiff neck
Diagnostic testing of CSF
Polymerase chain reaction (PCR) to detect viral-specific DNA/RNA
Symptomatic management with full recovery expected
Viral Meningitis
Acute inflammation of the brain
Sometimes fatal
Caused by viruses
Ticks or mosquits can transmit epidemic encephalitis
Cytomegalovirus (CMV) encephalitis is common in patients with AIDS
Encephalitis
Nonspecific
- Fever
- Headache
- Nausea, vomiting
Incubation period 3–14 days
Signs appear on day 2 or 4
- May vary from minimal alterations to coma
Hemiparesis
Tremors
Seizures
Cranial nerve palsies
Hemiparesis
Tremors
Seizures
Cranial nerve palsies
Encephalitis:Clinical Manifestations
CT
MRI
PET
PCR test for HSV DNA/RNA
Blood test for West Nile viral RNA
Encephalitis:Diagnostic Studies
Mosquito control for prevention
Acyclovir (Zovirax), ganciclovir (Cytovene) for HSV infection (start before onset of coma)
Antiseizure medications for seizures
Encephalitis: Nursing and Interprofessional Management
Accumulation of push within brain tissue
Streptococci and Staphylococcus aureus are causative organisms
Headache
Fever
Nausea, vomiting
Signs of increased ICP
Symptoms reflect local area of abcess
Brain Abscess
Primary – arising from tissues within the brain
Secondary – from metastasis
Brain tumour
Commonly classified as peripheral neuropathies
Disorders usually involve motor, sensory, or both
Causes include:
Tumours
Trauma
Infections
Inflammatory processes
Unknown causes
Cranial nerve disorders
Average age of onset is 60
Rarely diagnosed in people less than 40
Women more often than men
Pathophysiology not fully understood
Trigeminal Neuralgia
Abrupt onset of:
Paroxysms of flashing
Stabbing pain
Attacks are usually brief
Usually initiated by a triggering mechanism
Chewing
Brushing teeth
Hot/cold air
Trigeminal Neuralgia
Anticonvulsive medications – Tegretol
First line of treatment
Acts on sodium channels to lengthen neuron repolarization and therefore decreased neuron firing.
S/E - Blood abnormalities from bone marrow suppression
Antispasmodics – Baclofen
Can be given with the anticonvulsant medication or on its own
Reduces pain
Other anticonvulsants – gabapentin
OTHER TREATMENT
Analgesic blocks – pain relief for 6 – 18 months
Biofeedback
surgery
Trigeminal Neuralgia - Drug Therapy
Disorder characterized by disruption of the motor branches of CN VII
One side of the face
Absence of other disease such as stroke
Exact etiology unknown
Immune
Infective ischemic mechanisms
Acute onset
Unilateral facial paralysis affecting muscles of the upper and lower face
Diagnosis is based on clinical presentation.
Corticosteroid treatment
Bell’s Palsy
Acute, rapidly progressing polyneuritis
Manifests as symmetrical ascending paralysis from the results in loss of myelin, inflammation and edema of the affected nerves.
Etiology is unknown but thought to result from an immunological reaction.
EMG and nerve conduction studies show evidence of demyelination.
Lumbar Puncture may show elevated protein 10 days after the onset of symptoms.
Guillain-Barre Syndrome
Acute phase – patient is in the ICU
Patient is at risk for:
- Respiratory problems and infection.
Anxiety
Nutritional deficiencies
Skin breakdown
Pain management
Communication difficulties
Fluid and electrolyte disturbances
Recovery phase - involves intense long term rehabilitation.
Guillain-Barre Syndrome
An acute neurological disorder that causes life threatening neuroparalysis
From a spore forming bacterium – clostridium botulinum, that produces a neurotoxin
The toxin destroys or inhibits the neurotransmission of acetylcholine at the myoneural junction
A reportable disease
Symmetrical descending motor paralysis no sensory deficits
Treatment IV botulinum antitoxin
Gastric lavage, laxatives, to decrease the absorption of toxin – must not have magnesium because it worsens toxin induced neuro muscular blockade.
BOTULISM
inflammation of the nerve roots and polyneuritis occurs from a neurotoxin produced by clostridium tetani.
Spores are present in the soil, garden mould and manure
Enters the body through a wound
Incubation period 3 - 21 days
Stiffness in the jaw or neck; symptoms of infection like fever, malaise,
Progresses to other areas causing increased rigidity
If progresses, then opisthotonos (extreme arching of the back and retraction of the head) during convulsion
Symptoms of an over stimulated sympathetic nervous system – diaphoresis, labile hypertension, tachycardia, hyperthermia, dysrhythmias.
Seizures with slight stimulation like lights, motions noise.
Managed with tetanus and diphtheria toxoid booster and tetanus immune globulin
Tetanus
Caused by treponema pallidum organism which invades the central nervous system
Fatal if not treated.
Can occur at any time during the course of syphilis
Late symptoms include degenerative changes in the spinal cord (tabes dorsalis) and the brain stem (general paresis).
Charcot joints - enlarged hypermobile joints with bone destruction
Seizures, vision and hearing impairment
Neurological and psychiatric symptoms
Penicillin, symptomatic care
Neurosyphilis
Can have a devastating effect on health and well-being
SCI is divided into traumatic (result of external physical impact) and non-traumatic (result of disease, infection, or tumour) categories
Spinal Cord Injuries
Primary injury (initial injury) to the spinal cord.
Cord compression
Initial injury disrupts axons, blood vessels and cell membranes
Etiology and Pathophysiology- Spinal Cord Injury
Secondary injury
Ongoing, progressive damage that occurs after initial injury
Apoptosis may occur weeks to months after the initial injury
Ischemia, hypoxia, microhemorrhage and edema.
Etiology and Pathophysiology- Spinal Cord Injury
Temporary neurological syndrome
Characterized by
Decreased reflexes
Loss of sensation
Flaccid paralysis below level of injury
Experienced by about 50% of people with acute spinal cord injury
Spinal shock
Loss of vasomotor tone caused by injury
Characterized by hypotension, hypothermia, and bradycardia (important clinical cues)
Loss of sympathetic nervous system innervation causes
Peripheral vasodilation
Venous pooling
Decreased cardiac output
Neurogenic shock
Classified by mechanism of
Injury
Most are related to flexion, hyperextension, flexion rotation, extension-rotation and compression
Skeletal level of injury
Neurological level of injury
Completeness or degree of injury
Spinal and Neurogenic ShockClassification of Spinal Cord Injury
Skeletal injury at the vertebral level
Tetraplegia or paraplegia
Neurological level is the lowest where sensory and motor function are both normal
Level of Injury
Damage to central spinal cord either complete or incomplete
Motor weakness and sensory loss are present in both upper and lower extremities.
6 syndromes
Central cord syndrome
Anterior cord syndrome
Brown-Sequard
Posterior cord syndrome
Cauda equina syndrome
Conus medullaris syndrome
Degree of InjuryCentral Cord Syndrome
motor problems, temperature problems – below the injury, touch remains in tact (position, vibration & motion)
Anterior cord syndrome
remain in tact with anterior idk what she said that was fucked
Posterior tract
Results from cord compression, ischemia, edema , cord transection (rare)
Symptoms are related to the level and degree of the injury
The higher the injury the more serious
Combined motor and sensory symptoms
Clinical Manifestations - Spinal Cord Injury
Respiratory
- total loss of respiratory muscle function above level of C4
Cardiovascular
- bradycardia
Urinary System
- retention
Gi System
- injury above T5 leads to gastric hypomotility
Integumentary
- high risk of skin breakdown
Metabolic
- loss of body weight
- high nutritional needs
Thermoregulation
- poikilothermic
Peripheral Vascular
- DVT, PE
Clinical Manifestations - Spinal Cord Injury
CT scan may be used to assess stability of injury, location, and degree of bone injury.
MRI is gold standard for imaging neurological tissues.
Comprehensive neurological examination
Assessment of head, chest, abd for additional injuries or trauma
Vertebral angiography if there is altered mental status – to rule out vertebral artery damage.
Diagnostic studies
Immediate goals are to sustain life and prevent further cord damage.
Patent airway
Adequate ventilation
Adequate circulating blood volume
Systemic and neurogenic shock must be treated to maintain BP.
Thoracic and lumbar vertebrae injuries
Systemic support less intense than cervical injury
Respiratory compromise not as severe
Bradycardia is not a problem.
Specific problems treated symptomatically
After stabilization, history is obtained.
Emphasis on how injury occurred
Extent of injury as perceived by client immediately after event
Collaborative Care
Assessment
Test muscle groups with and against gravity, alone and against resistance, and on both sides of the body.
Note spontaneous movement.
Sensory examination
Position sense and vibration
Brain injury may have occurred—assess history for
Unconsciousness.
signs of concussion.
increased intracranial pressure.
Musculo-skeletal injuries
Trauma to internal organs
Collaborative Care
Focused on stabilization of injured spinal segment and decompression
Through traction or realignment
Eliminates damaging motion at injury site
Intended to prevent secondary damage
NON-OPERATIVE STABILIZATION
Cord decompression may result in decreased secondary injury.
Evidence of cord compression
Progressive neurological deficit
Compound fracture
Bony fragments
Penetrating wounds of spinal cord or surrounding structures
CRITERIA FOR EARLY SURGERY
Methylprednisolone (MP)
When administered early and in large doses, recovery of neurological function is greater.
May be used as a treatment option
No benefit after 8 hours post injury
Vasopressor agents
Used in acute phase
Maintain mean arterial pressure
Pharmacological agents
Used to treat specific autonomic dysfunctions
Collaborative CareDrug Therapy
Past health history
Current medication history
Symptoms
Loss of strength, movement and sensation below level of injury
Dyspnea, “air hunger”
Pain
Fear, denial, anger, depression
Subjective data - Spinal Cord Injury
General: poikilothermism
Integumentary: neurogenic shock
Respiratory: lesions at C1-C3, C4 and C5-T6
Cardiovascular: lesions above T5
GI: decreased or absent bowel sounds
Urinary: retention, flaccid bladder
Reproductive: priapism, loss of sexual function
Neurological: Complete, incomplete
Musculo-skeletal: atony, contractures
Objective data - Spinal Cord Injury
Ineffective breathing pattern
Imbalanced nutrition: less than body requirements
Ineffective peripheral tissue perfusion
Impaired skin integrity
Constipation
Impaired urinary elimination
Constipation
Impaired urinary elimination
Risk for autonomic dysreflexia
Nursing diagnosis
Overall goals
Maintain an optimal level of neurological functioning.
Have minimal to no complications of immobility.
Learn skills, gain knowledge, and acquire behaviours to care for self.
Return to home and community.
Planning
Proper immobilization involves maintenance of a neutral position.
Stabilize neck to prevent lateral rotation of cervical spine.
A blanket or towel
Hard cervical collar
Backboard
Body should always be correctly aligned.
Turn client so that he or she is moved as a unit to prevent movement of spine (log rolling).
Immobilization
Cervical collars for postsurgical stabilization are used on the basis of surgeons’ preference.
With new techniques and better surgical stabilization, a collar is not required postoperatively.
Halo traction is the most commonly used method of stabilizing cervical injuries.
Hanging weights may be incorporated.
May be attached to a body vest that allows ambulation.
Immobilization
Massive uncompensated cardiovascular reaction mediated by sympathetic nervous system
Occurs in response to visceral stimulation
Life-threatening
Most common precipitating factor is distended bladder or rectum.
Manifestations
Hypertension
Blurred vision
Throbbing headache—take BP
Marked diaphoresis above lesion level
Bradycardia
Autonomic Dysreflexia
Manifestations (cont.)
Piloerection (erection of body hair) resulting from pilomotor spasm
Flushing of skin above lesion
Spots in visual field
Nasal congestion
Anxiety
Nausea
Autonomic Dysreflexia
Nursing interventions
Elevate head of bed at 45 degrees, or sit client upright.
Notify physician.
Assess cause.
Provide immediate catheterization.
Teach client and family causes and symptoms.
Autonomic Dysreflexia
Any type of bladder dysfunction related to abnormal or absent bladder innervation
Common problems
Urgency, frequency, incontinence, inability to void, and high bladder pressures resulting in reflux of urine into kidneys
Neurogenic Bladder
Voluntary control may be lost.
High-fibre diet and adequate fluid intake
Suppositories, small-volume enemas, or digital stimulation by client or nurse
Carefully record bowel movements.
Neurogenic Bowel
Prevention of pressure ulcers and other types of injury to insensitive skin is essential.
Teach these skills and provide information about daily skin care.
Careful positioning and repositioning should be done every 2 hours with gradual increase in time
Pressure-relieving cushions must be used in wheelchairs.
Protect skin by avoiding thermal injury.
Teach family members skin care as well.
Neurogenic Skin
Important issue regardless of client’s age or gender
Nurse must
have an awareness and an acceptance of personal sexuality.
have knowledge of human sexual responses.
use medical terminology.
Injury level and completeness of injury are needed to understand the male client’s potential for orgasm, erection, and fertility, and the client’s capacity for sexual satisfaction.
Treatments for erectile dysfunction include drugs, vacuum devices, and surgical procedures.
Effects of spinal cord injury on female sexual response are less clear.
Woman of child-bearing age remains fertile and can become pregnant or to deliver normally through birth canal.
Sexuality
May feel an overwhelming sense of loss
May believe they are useless and burdens to their families
Response and recovery differ from those experiencing loss from amputation or terminal illness.
Grief and Depression
Spinal cord injury clients are living much longer lifespans.
Aging has serious impact on the older adult with a spinal cord injury.
Health promotion and screening are important.
Age-Related Considerations
Effects of musculoskeletal changes range from mild discomfort and decreased ability to perform activities of daily living (ADLs) to severe, chronic pain and immobility.
Decreased muscle mass and strength; loss of elasticity in ligaments, cartilage; joint problems; decreased bone density
Osteopenia and osteoporosis
Age-Related Considerations: the Musculoskeletal System
Subjective data
Important health information
Past health history
Medications
Surgery or other treatments
Objective data
Physical examination
Inspection
Palpation
Motion
Muscle-strength testing
Measurement
Other
Reflexes
Assessment of the Musculoskeletal System
Radiological studies
X-ray, CT, MRI, arthrogram, discogram
Bone mineral density (BMD) measurements
Radioisotope studies
Endoscopy
Mineral metabolism
Serological studies
Muscle enzymes
Invasive procedures
Arthrocentesis
Electromyogram (EMG)
Miscellaneous
Thermography
Somatosensory evoked potential (SSEP)
Diagnostic studies - Musculoskeletal System
Joint aspiration
Preformed to obtain synovial fluid sample or inject medications
Fluid is examined grossly for volume, colour, clarity, viscosity, and mucin clot test.
Arthrocentesis and Synovial Fluid Analysis
Acute (hours to days)
Impaired attention, awareness and cognition
Imbalance in neurotransmitters related to inflammation, hypoxia, and other biological and physiological factors
Inattentiveness and poor memory
Variable affect
Delirium
Insidious (months to years)
Slow progression
Gradual change in consciousness
Poor memory
Variable affect
Dementia
Variable onset
Variable onset
Worse in the morning and improves throughout the day
No change in consciousness
Difficulty concentrating, memory mostly intact
Depressed affect, loss of interest and pleasure.
Depression
Hyperactive delirium, hypoactive or mixed
Often mistaken for dementia
Delirium usually resolves within 4 – 7 days
Identification of the underlying cause is urgent
Delirium workup: complete blood count, biochemistry, thyroid levels, blood, urine and sputum cultures, oxygen sat, U/A chest Xray, EKG, possible CT scan of brain
Delirium
Foster orientation
Provide appropriate stimulation
Facilitate sleep
Foster familiarity
Maximize mobility
Reassure and educate patient and family.
Therapeutic Environment
Four most common in adults
Alzheimer’s disease
Vascular dementia
Dementia with Lewy bodies
Frontotemporal dementia
NOT A NORMAL PART OF AGING
Dementia
A collection of symptoms caused by various diseases affecting the brain
Memory
Judgement
Reasoning
Ability to communicate
Recognition
Mood and behavior
Cognition effects
Dementia
Problems disrupt the individual’s
Work
Social responsibilities
Family responsibilities
Activities of daily living (ADLs)
Dementia occurs most often in older persons.
Dementia
Part of later stages of Parkinson’s disease and Huntington’s disease
Individuals with Down syndrome have higher risk of developing dementia, and at a younger age.
Creutzfeldt-Jakob disease (CJD)
Dementia
Some treatable conditions
Delirium, depression, subdural hematoma, cerebral tumours, normal-pressure hydrocephalus, heavy metal toxicity, Wilson’s disease, and some infections (e.g., bacterial meningitis)
Etiology and Pathophysiology
Chronic progressive, degenerative disease of the brain
Most common form of dementia
Familial AD
Alzheimer’s Disease
Changes in brain structure and function
Amyloid plaques
Neurofibrillary tangles
Loss of connections between cells and cell death
Alzheimer’s Disease:Etiology and Pathophysiology
People develop some plaques in their brain tissue.
In AD plaque is greater in certain parts.
Clusters of insoluble plaque
β-amyloid, other proteins, remnants of neurons, non-nerve cells, and other cells
Alzheimer’s Disease: Etiology Pathophysiology
Where plaques develop in the parts of the brain used for
- memory
- cognitive function
Eventually develops in the cerebral cortex
Neurofibrillary tangles
- Abnormal collections of twisted protein threads inside nerve cells
- The main component is a protein called tau.
Gradual loss of connectiosn between neurons
- Leads to damage and then death of neurons
Affected parts of brain shrink
- Brain atrophy
- Significant shrinkage in final state of AD
Alzheimer’s Disease:Etiology and Pathophysiology
Results from ischemic, ischemic-hyoxic or hemorrhagic brain damage
Can be caused by a single infarct or by multiple strokes
Incidence increases with age
Risk factors include smoking, HTN, cardiac diseases, diabetes, hypercholesterolemia, coronary artery disease and atrial fib.
Vascular Dementia
Degenerative changes in the frontal lobe, temporal lobe or both.
4 different variants – most common is the behavioural and the language variant from the effects on the frontal and temporal lobes.
Cell death occurs from the accumulation of proteins in the neurons – ubiquitin and TDP-43.
Small percentage is inherited (10%)
Age of onset is 52 – 56 years
Frontotemporal Dementia (FTD)
Presence of deposits of a synuclein protein (Lewy bodies) in the cortex, brainstem and autonomic structures.
Changes in thinking, reasoning, confusion, memory loss, balance problems and muscle rigidity)
Dementia with Lewy Bodies (DLB)
Creutzfeldt-Jakob disease (CJD)
Rare and fatal brain disorder
Caused by a prion protein
Very rare
Caused by prion protein
Mad cow disease
Creutzfeldt-Jakob Disease (CJD)
8 A’s - Dementia
- Attentional deficits
- Apathy
- Amnesia
- Altered perception
- Apraxia
- Aphasia
- Agnosia - unable to recognize and identify objects, persons, or sounds using one or more of their senses despite otherwise normally functioning senses
- Anosognosia – unaware of own disability
Pathological changes precede clinical manifestations 3-20 years
Categorized similarly to those for dementia
- mild (early)
- moderate (middle)
- severe (late)
Dementia:Clinical Manifestations
Early signs of Dementia
Mild forgetfulness
Impairment of Short-term memory
Difficulty recognizing what numbers mean
Loss of initiative and interests
Poor judgement
Difficulty finding the right word
Confusion about location of familiar places
Anxiety
Dementia:Clinical Manifestations - Mild
Middle (moderate)
Anxiety, mood swings, jealousy, irritability
Difficulty completing tasks, learning new things, recognizing family members, language, logic
Flat affect
Hallucinations, delusions
Impaired attention
Increasing memory loss
Loss of impulse control, interest in hygiene and remote memory
Poor insight
Sleep disturbances, wandering
Dementia:Clinical Manifestations - Moderate
Late (severe)
Aggressive behaviours
Difficulty eating, swallowing
Hallucinations, delusions, agitation
Inability for self-care
Inability to understand words
Incontinence
Loss of appetite, most memories, social skills
Progression to loss of facial expression
Repetitious words or sounds
Seizures
Sexual disinhibition
Dementia:Clinical Manifestations - severe
No single clinical test
Made once all other possible conditions causing cognitive impairment have been ruled out
Diagnosis of exclusion
Complete health history
Physical examination
Neurological assessment
Brief cognitive tests
Laboratory tests
Comprehensive patient evaluation
Neuropsychological testing and neuroimaging
Mental statu testing
(MMSE, MoCA, CICA)
MMSE
mini mental
MoCA
highly sensitive, need to be certified – she highly suggests we do the online one
CICA
Canadian Indigenous Cognitive Assessment
No cure
Interprofessional management aimed at
Improving or controlling decline in cognition
Maintaining and maximizing functioning and quality of life
Supporting family caregivers
Dementia: Interprofessional Care
AD is the only form of dementia for which medications that affect cognitive decline are approved by Health Canada.
Cholinesterase inhibitors
Block cholinesterase, enzyme responsible for breaking down acetylcholine
Improve or stabilize cognitive decline but do not cure or reverse disease
Increased risk of bradycardia and syncope
S/E nausea, vomiting, diarrhea, vivid dreams and let cramps.
DON’T CURE OR REVERSE PROGRESSION
Dementia: Medication Therapy
Memantine (Ebixa) protects nerve cells against excess amounts of glutamate.
- May be used if cholinesterase inhibitors are ineffective
- Recommended for moderate to severe AD
- Adverse effects include nausea, vomiting, diarrhea, vivid dreams, and leg cramps.
Antipsychotic medications used sparingly
Selective serotonin reuptake inhibitors (SSRIs)
- may help with sleep conditions
Antidepressants
Increased risk of delirium with psychiatric meds
Dementia: Medication Therapy
Self-neglect
Potential for injury
Wandering
Dementia: Nursing Diagnosis
Overall goals for patient
Maintain physical health
Retain functional abilities
Enhance or stabilize cognition
Eliminate pain
Prevent responsive and self-protective behaviours
Support emotional and physical well-being
Overall goals for family caregiver
Reduce caregiver stress.
Maintain health and well-being.
Partnership and collaboration with patients and families is essential.
Dementia: Planning
Health promotion
Strategies to prevent dementia
Early recognition
Exercise
Dementia: Nursing Implementation
INDIVIDUALS WITH DEMENTIA WHO ARE HOSPITALIZED, ARE AT A HIGHER RISK FOR _______ OUTCOMES.
NEGATIVE
Diagnosis is traumatic for patient & family
Pt often responds with:
- depression, denial, anxiety & fear, isolation, grieving
An important nursing responsibility is to work collaboratively w/ the patient’s caregiver to manage clinical manifestations effectively as they change over time
Acute Intervention: Dementia
Family members and friends care for most persons with dementia in their homes.
Various facilities should be evaluated.
Consider stage of dementia when choosing a facility.
Nursing care intensifies over time.
Dementia: Ambulatory & Home Care
In early stages, memory aids (e.g., calendar) may provide benefit.
Medications must be taken regularly.
Medication adherence can be challenging.
Advance care planning
Adult day care can provide
Caregiver respite
Stimulation for AD patient
Demands on the caregiver can exceed resources, and total care is needed.
The person with dementia may need to be placed in a long-term care facility.
Emphasis is on safety.
Dementia: Ambulatory & Home Care
Occur in 50-60% of patients
Often not persistent
Not intentional but a way of communicating
May communicate emotion
Behavioural & psychological symptoms of dementia (BPSDs) may worsen in acute care settings
Dementia: Behavioural Changes
Assess patient’s
Physical status
Environment
Reassure patient about their safety.
Nursing strategies to communicate effectively
Stay near the patient, use touch as appropriate
Adapt to patient’s rhythm
Focus on care
Other strategies
Redirection
Distraction
Reassurance
Dementia: Behavioural Changes
Sundowning
- behavioural disturbances
- behaviour should be assessed for the underlying cause
Nursing Interventions: Sundowning
- Create a quiet, calm environment.
- Maximize exposure to daylight.
- Uninterrupted nighttime sleep
- Sleep hygiene
- Engage patient in activities during the day.
Dementia:Behavioural Changes
Risks
Injury from falls
Wandering
Injury to others and self
Fire or burns
Impaired judgement and decision making
Vulnerability to elder abuse
The nurse can help the caregiver in assessing the home environment for safety risks.
Wandering is major concern.
Patients with dementia can register with Safely Home.
Dementia: Safety
Pain should be recognized and treated promptly.
Pain management is complex.
Monitor patient’s response.
Rely on other behavioural cues of pain and signs of distress.
Dementia: Pain management
Nutritional deficits
Loss of interest in food
Decreased ability to self-feed
Comorbid conditions
Dementia:Eating and Swallowing Difficulties
When chewing and swallowing become difficult, use
- pureed food
- thickening liquids
- nutritional supplements
Quiet and unhurried enviroment
Easy-grip utensils
Offer liquids frequently
Finger foods may enable self feeding
Short term possibilities
- alternate routes of nutrition other than oral
Dementia: Eating and Swallowing Difficulties
In late stages, the patient will be unable to perform oral self-care.
Dental conditions are likely to occur.
The patient may pocket food, adding to potential tooth decay.
Inspect the mouth regularly and provide mouth care.
Dementia: oral care
Common
Urinary tract infection
Pneumonia
Ultimate cause of death in many patients with dementia
Manifestations need prompt evaluation and treatment.
Dementia: Infection Prevention
In late stages, patients are at risk for skin breakdown.
Incontinence, immobility, and undernutrition
Treat rashes, areas of redness and skin breakdown.
Keep skin dry and clean.
Change patient’s position regularly.
Dementia Skin Care
Urinary and fecal incontinence during middle to late stages
Regular toileting or behavioural retraining may decrease episodes.
Constipation may relate to immobility, dietary intake, decrease in fluids.
Dementia Elimination Conditions
occurs when ischemia or hemorrhage into the brain results in death of brain cells.
Physical, cognitive, and emotional impact
Stroke
Most effective way to decrease the burden of stroke is prevention.
Risk factors can be divided into nonmodifiable and modifiable risks.
Asymptomatic carotid stenosis
Arteriovenous malformation (brain)
Hypertension
Diabetes mellitus
Heart disease
Alcohol consumption
Oral contraceptive use
Physical inactivity
Smoking
Obesity
Drugs
Hypercoagulability
Risk factors for stroke
Alcohol increases
BP
A Transient Ischemic Attack (TIA) is usually a precursor to ischemic stroke.
thrombotic
Transient ischemic attack (TIA)
Transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction of the brain
Symptoms last <1 hour.
Ischemic Stroke
Thrombotic stroke
Thrombosis occurs in relation to injury to a blood vessel wall and formation of a blood clot.
Result of thrombosis or narrowing of the blood vessel
Most common cause of stroke
Lacunar strokes are typically asymptomatic.
Ischemic Stroke
Embolic stroke
Occurs when an embolus lodges in and occludes a cerebral artery
Results in infarction and edema of the area supplied by the involved vessel
Second most common cause of stroke
Warning signs are less common with embolic than with thrombotic stroke.
Ischemic Stroke
Account for approximately 15% of all strokes
Result from bleeding into the brain tissue itself or into the subarachnoid space or ventricles
Hemorrhagic Stroke
Bleeding within the brain caused by rupture of a vessel
Hypertension is the most important cause.
Hemorrhage commonly occurs during periods of activity.
Often a sudden onset of symptoms, with progression over minutes to hours because of ongoing bleeding
Manifestations
Neurological deficits
Headache
Nausea and/or vomiting
Decreased levels of consciousness
Hypertension
Hemorrhagic Stroke - Intracerebral hemorrhage
Intracranial bleeding into cerebro-spinal fluid–filled space between the arachnoid and pia mater
Commonly caused by rupture of a cerebral aneurysm
An aneurysm may be saccular or berry.
Majority of aneurysms are in the circle of Willis.
“Worst headache of one’s life”
Surgical treatment to prevent rebleeding.
Affects many body functions
Motor activity
Elimination
Intellectual function
Spatial–perceptual alterations
Personality
Affect
Sensation
Communications
Hemorrhagic Stroke- Subarachnoid Hemorrhage
Obvious effect of stroke
Include impairment of
Mobility
Respiratory function
Swallowing and speech (dysphagia)
Gag reflex
Self-care abilities
Loss of skilled voluntary movement
Impairment of integration of movements
Alterations in muscle tone
Alterations in reflexes
Clinical ManifestationsMotor Function
Client may experience aphasia when a stroke damages the dominant hemisphere of the brain.
Aphasia is the total loss of comprehension and use of language.
Dysphasia refers to difficulty related to the comprehension or use of language and is due to partial disruption or loss.
Four categories
Expressive
Receptive
Anomic/amnesic
Global
Dysarthria of mechanisms of speech are affected.
Clinical Manifestations
Communication
Clients who suffer a stroke may have difficulty controlling their emotions.
Emotional responses may be exaggerated or unpredictable.
Clinical Manifestations
Affect
Both memory and judgement may be impaired as a result of stroke.
A left-brain stroke is more likely to result in memory problems related to language.
Clinical Manifestations
Intellectual Function
Spatial–Perceptual Alterations
Stroke on the right side of the brain is more likely to cause problems in spatial–perceptual orientation.
However, this may occur with left-brain stroke.
Clinical Manifestations
Spatial–Perceptual Alterations
Most problems with urinary and bowel elimination occur initially and are temporary.
When a stroke affects one hemisphere of the brain, the prognosis for normal bladder function is excellent.
Clinical Manifestations
Elimination
When symptoms of a stroke occur, diagnostic studies are done to
confirm that it is a stroke.
identify the likely cause of the stroke.
CT is the primary diagnostic test used after a stroke.
CTA
MRI, MRA
Cerebral or carotid angiography
Digital subtraction angiography
Transcranial Doppler ultrasonography
Lumbar puncture
Diagnostic Studies
Priority for decreasing morbidity and mortality from stroke
Goals of stroke prevention include
health promotion for the well individual.
education and management of modifiable risk factors to prevent a stroke.
Clients with known risk factors require close management.
Diabetes mellitus
Hypertension
Smoking
High serum lipids
Cardiac dysfunction
Collaborative Care
Prevention
Antiplatelet drugs are usually the chosen treatment to prevent further stroke in clients who have had a TIA.
Aspirin is the most frequently used antiplatelet agent.
Statins
Surgical interventions for the client with TIAs from carotid disease include
carotid endarterectomy.
transluminal angioplasty.
stenting.
extracranial–intracranial bypass.
Collaborative Care
Prevention
Goals for collaborative care during the acute phase are
preserving life.
preventing further brain damage.
reducing disability.
Treatment differs according to type of stroke and as client changes.
Begins with managing the ABC’s
Collaborative Care
Acute Care
Altered level of consciousness
Weakness, numbness, or paralysis
Speech or visual disturbances
Severe headache
↑ or ↓ heart rate
Respiratory distress
Unequal pupils
Hypertension
Facial drooping on affected side
Difficulty swallowing
Seizures
Bladder or bowel incontinence
Nausea and vomiting
Vertigo
Assessment
Interventions: initial
Ensure patent airway.
Call stroke code or stroke team.
Remove dentures.
Perform pulse oximetry.
Maintain adequate oxygenation.
Obtain IV access with normal saline.
Maintain BP according to guidelines.
Remove clothing.
Insert Foley catheter
Obtain CT scan immediately.
Perform baseline laboratory tests.
Position head midline.
Elevate head of bed 30 degrees if no symptoms of shock or injury occur.
Collaborative Care: Acute Care
Hypertension is common immediately after stroke.
Drugs to lower BP are used only if BP is markedly increased.
Fluid and electrolyte balance must be controlled carefully.
Adequate hydration promotes perfusion and decreases further brain injury.
Interventions: ongoing
Monitor vital signs and neurological status.
Level of consciousness
Motor and sensory function
Pupil size and reactivity
O2 saturation
Cardiac rhythm
Recombinant tissue plasminogen activator (tPA)
Used to reestablish blood flow through a blocked artery to prevent cell death in clients with acute onset of ischemic stroke symptoms
Must be administered within 3–4.5 hours of onset of clinical signs of ischemic stroke
Collaborative Care: Acute Care
After stroke has stabilized for 12–72 hours, collaborative care shifts from preserving life to lessening disability and attaining optimal functioning.
Client may be transferred to a rehabilitation unit, outpatient therapy, or home care-based rehabilitation.
Rehabilitation
If the client is stable, obtain
description of the current illness with attention to initial symptoms.
history of similar symptoms previously experienced.
current medications.
history of risk factors and other illnesses.
family history of stroke or cardiovascular disease.
Comprehensive neuro examination
Level of consciousness (using Canadian Neurological Scale)
Cognition
Motor abilities
Cranial nerve function
Sensation
Proprioception
Cerebellar function
Deep tendon reflexes
Nursing Assessment
Decreased intracranial adaptive capacity
Risk for aspiration
Impaired physical mobility
Impaired verbal communication
Unilateral
Impaired urinary elimination
Impaired swallowing
Situational low self-esteem
Nursing Diagnoses
Goals are that the client will
maintain stable or improved level of consciousness.
attain maximum physical functioning.
maximize self-care abilities and skills.
maintain stable body functions.
Maximize communication abilities.
Avoid complications of stroke.
Maintain effective personal and family coping
Planning
Unilateral (60%)
Throbbing
Periodic
Lasts 4-72 hours
Prodrome may be present
Aura
N&V, photophobia, irritability
Migraine
Bilateral
Constant
Squeezing
Cycles for many years
Lasts 30 min to 7 days
Palpable neck and shoulder muscles, stiff neck & tenderness
Tension
Unilateral w/ radiation up or down from one eye
Severe bone crushing
Attacks occur in clusters
Last 15-180 minutes
At night - commonly awakens people
Facial flushing, pallor, unilateral lacrimation, ptosis, and rhinitis
Cluster
TIPTANS – REDUCE NEUROGENIC INFLAMMATION OF THE CEREBRAL BLOOD VESSSESLS, AND PRODUCE VASOCONSTRICTION
NSAIDS, ASA caffein containing combinations
Migraine - Drug Therapy
-ASA, Tylenol, NSAIDS antidepressants
TENSION Drug Therapy
100% oxygen ,
Prophylactic treatment like topamax
CLUSTER Drug Therapy
Transient uncontrolled neuronal activity in the brain, interrupting normal function
Often symptom of underlying illness
Seizures resulting from metabolic disturbances are not considered epilepsy if seizures cease when underlying condition is treated.
Seizure
Condition in which a person has at least two spontaneous seizures >24 hours apart, caused by underlying chronic pathology
Affects approximately 0.6% of Canadians
75 to 85% of people with epilepsy receive a diagnosis before the age of 18 years.
Epilepsy
Seizure disorder is characterized by abnormal neurons undergoing spontaneous firing.
The cause of abnormal firing is unclear.
Firing spreads to adjacent or distant areas of the brain.
If activity involves the whole brain, generalized seizure occurs.
Astrocytes are now believed to play a key role in recurring seizures.
Etiology & Pathophysiology - Seizure
Determined by site of electrical disturbance
Generalized, focal or unknown
May progress through several phases
Prodrome phase
Aural phase
Ictal phase
Postictal phase
Seizures - Clinical Manifestations
Electric activity in one particular area (focal)
Unilateral manifestations
May be confined to one side of brain and remain partial or focal or may spread to involve the entire brain becoming a secondary generalized seizure
Includes focal aware seizures and focal impaired awareness seizures
Focal Seizures
Characterized by bilateral synchronous epileptic discharges in brain from seizure onset
Tonic Clonic – grand mal
Typical Absence seizures
Atypical Absence seizures
Atonic
Generalized Seizure
______ epilepticus is most dangerous as it can cause ventilatory insufficiency, hypoxemia, cardiac arrhythmias, hyperthermia, and systemic acidosis.
Trauma during seizures can cause severe injury and death.
Tonic–clonic status
Administered slowly to prevent acute hypotension
Serum albumin and phenytoin levels
Discontinued at first sign of rash and anticonvulsive treatment reassessed
Alcohol intake may affect phenytoin serum levels.
Phenytoin
Neurological assessment for dose-related _____ involves testing for
Nystagmus
Hand and gait coordination
Cognitive functioning
General alertness
toxicity
Vagal nerve stimulation gives intermittent stimulation to the brain to reduce the frequency and intensity of seizures
Responsive neurostimulation
Ketogenic diet
Biofeedback to control seizures teaches the patient to maintain a certain brain wave frequency that is refractory to seizure activity
Interprofessional Care
aura; focal sensory, motor, cognitive, or emotional phenomena; unilateral “marching”; motor seizure
Focal aware
altered consciousness with inappropriate behaviours, amnesia of event
Focal impaired awareness
Injury related to ligamentous structures surrounding the joint
1st degree, 2nd degree, 3rd degree
Sprain
Excessive stretching of a muscle
1st degree, 2nd degree, 3rd degree
Strain
Partial or incomplete displacement
Subluxation
Severe injury of the ligamentous structures around a joint
Complete displacement of the bone from its normal position.
Dislocation
A cumulative trauma disorder
Results from prolonged force or repetitive movements and awkward postures.
Repetitive Strain Injury (RSI)
Caused by compression of the median nerve.
Most common compression neuropathy in the upper extremity,
Weakness, burning sensation (causalgia), numbness, tingling
Positive Tinel and Phalen sign.
Carpal Tunnel Syndrome
Rotator cuff – 4 muscles (supraspinatus, infraspinatus, teres minor, and subscapularis muscle)
Tear in the rotator cuff in one of the 4 muscles.
Shoulder weakness, pain and decreased ROM
Increased pain when the arm is abducted 60 – 120 degrees.
Requires an MRI
Rotator Cuff Injury
Menisci are crescent-shaped pieces of fibrocartilage in the knee.
Associate with ligament strain.
A torn meniscus exhibits, localized tenderness, pain, and effusion
Meniscus Injury
An intact ACL requires conservative treatment such as rest, ice, NSAIDS and elevation, ambulation is usually as tolerated.
A torn ACL may require reconstructive surgery where the torn ACL tissue is replaced with autologous or allograft tissue.
Anterior Cruciate Ligament Injury
Inflammation of the bursa
Results from repetitive, or excessive trauma or friction, gout, rheumatoid arthritis or infection
Treated w/ rest, ice, NSAIDs, corticosteroid injections
Bursitis
Seen with muscle fatigue, overuse, dehydration and electrolyte abnormalities.
Muscle injury resulting in inflammation and edema which irritates nerve endings and stimulates strong muscle contraction
Can lead to constriction on other blood vessels and nerves, stimulating muscle spasm in other muscles
These can even displace broken bone, even causing fracture and other damage
Muscle Spasm
A dislocation is an orthopaedic emergency
Increased risk of AVN (avascular necrosis), the longer it is out of place - hip is susceptible
Compartment syndrome, vascular injury can occur after dislocation
Repaired w/ a closed or open reduction
Fractures
_____ can be classified
Open or closed
Complete or incomplete
Based on direction of fracture line
Displaced or nondisplaced
Fractures
Mechanism of injury associated with numerous signs and symptoms
Immediate localized pain
Decreased function
Inability to bear weight on or use affected part
Client guards and protects extremity.
Clinical Manifestations - Fracture
______ goes through a remarkable reparative process of self-healing (union).
Fracture hematoma
Granulation tissue
Callus formation
Ossification
Consolidation
Remodelling
Bone
Electrical stimulation and pulsed electromagnetic fields (PEMFs)
Stimulate _______ healing
Electric currents modify cell mechanisms, causing bone remodelling.
Electrodes are placed over skin or cast and are used 10–12 hours each day.
bone
Nonsurgical, manual realignment of bone fragments to previous anatomical position
Traction and countertraction manually applied to bone fragments to restore position, length, and alignment
Closed reduction (fracture)
Correction of bone alignment through surgical incision
Includes internal fixation with use of wires, screws, pins, plates, intramedullary rods, or nails
Open reduction (fracture)
Application of a pulling force to an injured or diseased part of body or extremity, while countertraction pulls in opposite direction
Two most common types of traction
Skin traction
Skeletal traction
Traction
Fracture alignment depends on correct positioning and alignment while traction forces remain constant.
Forces must be pulling in opposite direction to prevent client from sliding to end or side of bed.
Countertraction commonly supplied by client’s body weight or augmented by elevating end of bed
Imperative that nurse maintains traction constantly and does not interrupt weight applied to traction
Collaborative Care: Traction
