Test 4 Flashcards by Sydney Coopland

The brain consists of the ______, _____ & ______

cerebrum, brainstem, and cerebellum

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The ____ is composed of the right and left hemispheres

cerebrum

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Both hemispheres can be further divided into four major lobes.

Frontal
Temporal
Parietal
Occipital

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The ______ lobe controls higher cognitive function, memory retention, voluntary eye movements, voluntary motor movement, and expressive speech in Broca’s area.

frontal

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The _____ lobe contains integration of somatic, visual, and auditory data, and Wernicke’s area, which is responsible for receptive speech.

temporal

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The _____ lobe is composed of the sensory cortex, controlling and interpreting spatial information

parietal

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Processing of sight take place in the _____ lobe.

occipital

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The basal ganglia, thalamus, hypothalamus, and limbic system are also located in the ______

cerebrum

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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

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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

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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)

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Peripheral nervous system
Spinal nerves
Cranial nerves
Autonomic nervous system (ANS)

Structures & Functions of Nervous System

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Meninges
Skull
Vertebral column

Protective Structures

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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

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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

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may be done for someone who has NPH, high fever, headache – to check for infection, meningeal irritation

Lumbar puncture

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Electroencephalography (EEG)
Electromyography (EMG) and nerve conduction studies
Evoked potentials

Electrographic studies

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Carotid duplex studies
Transcranial Doppler ultrasonography

Combined Doppler and ultrasound studies

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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

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Factors that influence _____:
BP
Cardiac function
Intraabdominal pressure
Intrathoracic pressure
Body position
Temperature
Blood gases – especially CO2

Intracranial Pressure (ICP)

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Occurs at the initial time of an injury that results in:
displacement,
Bruising
Or damage of the three components.

Primary Injury

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Occurs after the primary injury:
Hypoxia
Ischemia
Hypotension
Edema
Increased ICP

Secondary Injury

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Total pressure exerted because of the combined total volume of the 3 components of the skull:
Brain Tissue
Blood
CSF

ICP

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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

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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

1. Attentional deficits 2. Apathy 3. Amnesia 4. Altered perception 5. Apraxia 6. Aphasia 7. Agnosia - unable to recognize and identify objects, persons, or sounds using one or more of their senses despite otherwise normally functioning senses 8. 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

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