Perception And Coordination

Perception and Coordination

More than 10 minutes of oxygen deprivation-brain death

Perception-conscious recognition and interpretation

Sources of Blood supply: 1. Internal carotid arteries-anterior circulation, ipsilateral hemispheres 2. Vertebral arteries-posterior circulation, posterior fossa

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

White matter-less perfusion (bundles of fibers, terminal ends) Gray matter-more perfusion (body of neurons)

Coordination-when action or reaction towards a

•Circle of Willis

•

stimulus is occurring in a purposeful, orderly fashion, appropriate response to a stimulus Role of Nervous System: 1. Reciprocally interact with the environment 2. Maintain homeostasis (with the endocrine system)

•

Function: 1. Sensory-interpret incoming message 2. Integrative-analyze, store, make decisions regarding appropriate behavior 3. Motor-initiating muscular or glandular activity; ongoing and evolving interaction with environment

act as a safety valve; arises from basilar arteries and internal carotid arteries; vascular network at the base of the brain is important to total brain circulation because it provides equal circulation bilaterally. If one side of the circle of Willis is unable to supply adequate blood, the other side provides blood to the area normally supplied by the damaged side (Phipps, 1998, p. 1892)

•Cerebral arteries (2 each): Anterior, Middle, Posterior

•Jugular veins-drains the brain venous blood through dural sinuses

Ventricles and CSF • •

Ventricles- four fluid-filled cavities within the brain that connect one another and with the spinal canal CSF- form in the choroids plexus; about 135 cc o o o

Cushions Provide nutrients Allow fluid shifts

Special characteristics of Cerebral Perfusion 1.

3 essential components of skull: 1. Brain tissue-78% 2. Blood -12 % 3. CSF-10%

•

Monro-Kellie Hypothesis

SBP + 2 (DBP) 3 SBP-Systolic blood pressure DBP-Diastolic blood pressure • Cerebral perfusion pressure needed to ensure blood flow to the brain CPP=MAP-ICP

Normal Compensatory Adaptations: Initial: o Increases CSF absorption

o

Displacement of CSF into the spinal subarachnoid space—space between arachnoid and pia mater) Collapse of the cerebral veins and dural sinuses

Other mechanisms: o Distensibility of the dura o Increased venous outflow o Decreased CSF production o Constriction and vasodilation o Slight compression of brain tissue

Cerebral Blood Flow • • •

Amount of blood in milliliters passing through 100g of brain tissue in 1 minute Global CBF-approximately 50 ml/min Brain needs constant supply of oxygen and glucose (20% of body’s oxygen, 25% of body’s glucose)

Mean arterial pressure at which autoregulation is effective (70-105 mmHg) -Upper limit is 150 mmHg MAP=

If volume added to the cranial vault equals the volume displaced from it, the total intracranial volume will not change Normal ICP: 60-150 mmH20 or 0-15 mmHg

o

Autoregulation • 3 Physiologic mechanisms under normal circumstances: o Changes in intracranial pressure o Cerebral vasodilation o Metabolic factors

•

2.

As CPP decreases, autoregulation fails and CBF diminishes -30 mmHg is incompatible with life

Blood brain barrier • physiologic barrier between blood capillaries and brain tissue

NEUROPHYSIOLOGY Neurotransmission-conduction of an impulse throughout the nervous system Neurons • Receive and transmit impulses; non-mitotic • Excitable, conductive and can influence other cells

•

Parts: cell body (soma), dendrites (short) and axon Myelinated and unmyelinated

• Note:

When injured, centrally located neurons are unable to reproduce themselves because most cell bodies are located centrally and nerve cell bodies cannot reproduce. However, nerve endings can regenerate (Phipps, 1998, p. 1887). I.

Transmission within the Nerve fiber Action potential • Chemical gradient

• Electrical gradient Propagation of Action Potential 1. Resting stage (positive outside, negative inside) 2. Depolarization phase (negative outside, positive inside) II. Transmission across Synapse Synapses-small gaps between neurons • Chemical or electrical

•

Cranium and Cerebral column • Cranium-composed of 8 cranial and facial bones • Foramen magnum-largest hole through which the brain stem extends to the spinal cord • Vertebral column-protects the spinal cord, supports the head and provides flexibility; strengthened by ligaments and fibrocartilage disc

Cranial meninges • Dura mater • Arachnoid • Pia mater Falx cerebri-divides the left from right hemispheres Subdural-more bleeding

Central Nervous system: I.

One-way junction 1. Impulses reaches the presynaptic terminal 2. Vesicles release neurotransmitters 3. Neurotransmitters inactivated to prevent sustained response

Neurotransmitters-can be excitatory or inhibitory) Types: 1. Acetylcholine-muscle movement 2. Biogenic amines (thinking process) -Dopamine -Serotonin -Norepinephrine -Histamine 3. Amino acids -GABA -Peptides Neuroglia-protect and nourish neurons; mitotic - do not transmit impulses Neuroglia Function Astrocytes Supply nutrients to neurons Microglia Provide protection against microorganisms Oligodendrocytes Wrap tightly around nerve fibers to form myelin sheath Ependymal cells Ciliated; line brain cavities; forms CSF Schwann cells Phagocytic cells that form myelin sheath around nerve fibers Satellite cells Found in the PNS; may maintain chemical balance of neurons

Cerebrum a. Consists of 2 hemisphere b. Corpus callosum-connects two hemisphere c. Cerebral cortex-outer surface of the cerebrum d. Basal ganglia-located deep within cerebral hemisphere e. Internal capsule-white matter consisting of bundle of nerve fibers carrying motor and sensory impulses to and from cerebral cortex Lobes of the Cerebrum and their Functions Area

Frontal Primary motor area Speech area (Wernick’s ) Located in the posterior part of the superior temporal convolution Motor area (Broca’s) Located in the lateral, inferior portion of the frontal lobe Temporal Parietal

Occipital

II.

III.

Functions Controls movements of voluntary muscle Facilitates voluntary movement of skeletal muscle Understanding of spoken and written words

Promotes vocalization of words

Receives and interpret olfactory and auditory stimuli Promotes recognition of pain, coldness, light touch (Contralateral reception) Receives and interprets visual stimuli

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

• •

• •

IV.

V.

Midbrain-center for auditory and visual reflexes Pons-contains the fiber tracts; contains nuclei that controls respiration -contains pneumotaxic center—controls rhythmic quality of respirations Medulla-control cardiac rate, BP, respirators and swallowing Reticular activating system (RAS)-influence excitatory and inhibitory control of motor neuron; regulatory system for consciousness

Cerebellum • Has two hemispheres • Coordination of skeletal muscle activity, maintenance of balance, posture and control of voluntary movements Spinal cord • • •

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Somatic Nervous system • • •

• •

Controls involuntary or automatic body functions Has two subdivisions, serving same organ but have counterbalancing effects; each system can inhibit the organ stimulated by the other

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Sympathetic Nervous System  originates from lateral horns of first thoracic through the first lumbar of spinal cord (thoracolumbar)  helps the body cope with events in the external environment  Functions mainly during stress, triggering the fight or flight response  Increases heart rate and respiratory rate, pupil dilation, cold, and sweaty palms

•

Parasympathetic Nervous System  Consist of the vagus nerves originating in the medulla of the brain stem and spinal nerves originating from the sacral region of the spinal cord (craniosacral)  Activates GI system  Supports restorative, resting body function through such actions as replenishing fluids and electrolytes

Divisions: Ascending (Spinocerebellar) • Carry a specific sensory information to higher levels of CNS • Spinocerebellar tracts-muscle tension and body position • Spinothalamic-pain and temperature sensation

VI.

Reflex arc • •

Reflexes-automatic action; spinal cord mediates most reflexes Automatic or perceptible, inhibited or conditioned • Hyperreflexia-disease or injury of certain descending motor tracts • Hyporeflexia-damage or degeneration of the sensory or motor neurons

Peripheral Nervous system • •

Cranial nerves-innervate head and neck region, except the vagus nerve Spinal nerves • Plexuses-complex cluster of nerve fibers (cervical, brachial, lumbar and sacral region)

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

Autonomic Nervous System

Extends from medulla up to first lumbar vertebra Gives rise to 31 pairs of spiral nerves (C1C8, T1-T12, L1-L5, S1-S5, coccygeal nerve) Center for conducting messages to and from the brain; a reflex center

Descending (Corticospinal) • Pyramidal tracts-from the cortex to cranial and peripheral nerves; inhibits muscle tone • Extrapyramidal tracts-from brain stem, basal ganglia, and cerebellum; maintains muscle tone and gross body movements • Upper motor neurons-from cerebral cortex to anterior gray column of SC; spasticity and hyperactive reflexes • Lower motor neurons-“final common pathways” from anterior gray column up to muscles; flaccidity and loss of reflexes

Dermatomes-area of the skin innervated by cutaneous branches of a single spinal nerve

Effect organ Heart Lungs GIT • Motility • Tone sphincter s Urinary bladder • Bladder muscle • Sphincter Liver

Sympathetic Increased rate and contractility Relaxation

Parasympathetic Decreased rate and contractility Contraction

Decreased Contraction

Increased Relaxation

Relaxation

Contraction

Contraction Glycogenolysis

Relaxation None

Sensory System (General and special) Type of 1. 2. 3. 4. 5. 6. 7. 8. 9.

receptors: Exteroreceptors Interoreceptors Proprioceptors-specific receptors to detect balance, sense of position Mechanoceptors-detect pressure, touch (any stimulus that is physical in nature) Thermoreceptors-any changes in temperature Photoreceptors-light stimulus Chemoreceptors-taste, olfactory, pancreatic enzymes Nociceptors-severe stimulus Cutaneous receptors-touch

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Special senses:

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Sense of Sight

• • •

Collect light waves and transmit them as impulses to the brain, which translate them into images Normally form of a clear retinal image of an object at 20 ft. away Binocular vision—ability to judge relative, distances of objects

Decibels(dB)-unit of measure of intensity of sound Normal conversation= 65 dB Amplified rock music= 120 dB Nearby jetplane= about 140 dB Pitch •Corresponds to frequency; the higher the frequency the higher the pitch of the sound •Humans can potentially hear sounds whose frequency range from 16 to 2000 Hz •Upper range decreases slight with increasing age •Speech falls in the range of 85-1050 Hz

Anatomical features of the Eyeball Outer: 1. Cornea-thin, tough, transparent layer supplied with sensory nerve (touch and pain), no blood supply, oxygen and glucose through diffusion 2. Sclera Middle: 1. Choroid –highly vascular, dark brown membrane 2. Ciliary body-contract and dilate ciliary process which contain capillaries that secrete fluid 3. Iris-visible colored part of the eye; controls pupil size Inner: 1.

Retina-neural tissue, phagocytic, stores Vit. A, contains rods and cones Fovea-responsible for highly colored vision

2.

Refraction •

bending of light when it meets surfaces of different medium

Refractory media of the Eye 1. Cornea-performs most of the refraction because of its convex form

2. 3. 4.

Aqueous humor-fluid at the anterior and posterior chamber of the anterior cavity Crystalline lens-greatest refractive power Vitrous humor- thick, gelatinous fluid found at posterior chamber, give spherical shape to the eye

Physiology of Vision Formation of an image on the retina accomplished by the following: 1. Refraction 2. Accomodation 3. Constriction of pupils 4. Convergence of eyeballs Stimulation of retina •Dim light causes breakdown of the chemical rhodopsin present in rods •Cones-responsible for daylight and color vision •Perception of color is dependent on the cones •Most cones concentrated on fovea centralis •Condition to central area in occipital lobe •

Sense of Hearing Parts of the ear 1. Outer-collects sound 2. Inner-conducts sound •Eustachian tube • joins the middle ear and nasopharynx • transmit sound waves and maintain equilibrium Interpretation of sound

Loudness- Neurologic or psychologic interpretation of intensity; the greater intensity of the sound waves stimulating the organ of Corti, the greater will be the size of nerve impulses

Physiology of Hearing 1. Sound waves moving through the air enter the canal and move down to it to strike against the tympanic membrane causing it to vibrate 2. Vibrations of the tympanic membrane move the malleus

3. 4. 5. 6.

Movement of the malleus to the incus As the incus moves, it moves the stapes against the oval window, it starts a ripple on the perilymph Movement of the perilymph is transmitted to the endolymph muscle inside the cochlear duct and stimulates the organ of Corti Cochlear nerve conduct impulses from the organ of Corti to the brain; hearing occurs when impulses reaches auditory area in the temporal lobe of cerebral cortex

Mental Status Examination • An indication of how patient is functioning as a whole 1. 2.

3. 4. 5.

and how the patient is adapting to the environment General appearance State of consciousness • Arousal component • Content component Mood and effect-changes in the nervous system Thought content Intellectual capacity

NEUROLOGIC ASSESSMENT I.

Comprehensive History Taking • Demographic Data • Current health • Past health history • Medication history

• II. III.

Growth and development • Family health history • Psychosocial history V/S Mental Status Assessment • LOC • Orientation • Memory • Mood/affect • Intellectual performance • Judgment/Insight • Language/communication

IV. V. VI. VII.

Motor System assessment-muscle strength, tone, coordination, gait and station movement Sensory Function-superficial sensation, touch/pain, temperature, proprioception, discrimination Reflex activity Cranial nerve testing

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Cranial nerve III, IV, VI (Oculomotor, Trochlear, Abducens)-motor nerves that arise from the brainstem 1. Nystagmus –- involuntary eye movement; strokes of anterior, inferior, superior, cerebellar arteries 2. Constricted pupils: may signify impaired blood flow to vertebralbasilar arteries.

3.

MENTAL STATUS ASSESSMENT WITH ABNORMAL FINDINGS

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Unilateral neglect (lack of caring of the other side of the body); strokes involving middle cerebral artery. Poor hygiene and grooming: dementing disorders

Disorientation to time and place: stroke of right cerebral hemisphere 1. Memory deficits 2. Emotional defense

CRANIAL NERVE ASSESSMENTS

•

•

3.

Aphasia-defective or absent language function: TIA’s, strokes involving anterior/posterior artery; general term for impairment of language Dysarthria- (different in speaking); is indistinctness of words in word articulation resulting from interference with the peripheral speech mechanisms (e.g. muscles of the tongue, palate, pharynx, or lips) [Phipps, 1998, p. 1901] Decreased level of consciousness Confusion, Coma

2. 3. Note:

• •

Homonymous hemianopia - impaired vision or blindness in one side of both eyes; blockage of posterior cerebral artery. Impaired vision: strokes of anterior cerebral artery; brain tumors Visual acquity-mediated by the cones of the retina Field of vision or peripheral vision-portion of space in which objects are visible during the fixation of vision in one direction. The receptors for peripheral fields are the rod neurons of the retina. (Phipps, 1998, p. 1906)

Loss of facial sensation: contraction of masseter and temporal muscles, lesions CN V Severe facial pain: trigeminal neuralgia (tic dorlourex)

4.

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•

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Cranial I (Olfactory): Anosmia 1. lesions of frontal lobes 2. impaired blood flow to middle cerebral artery. Cranial II (Optic) 1. blindness in eye: strokes of internal carotid artery, TIA’s

Decreased sensation of face and cornea on same side of body; strokes of posterior inferior cerebral artery Lip and mouth numbness

2.

Emotional swings, personality changes: strokes

Dysphonia- change in tone of voice

Cranial nerve V (Trigeminal)—largest cranial nerve with motor and sensory components: changes in facial sensations; impaired blood flow to carotid artery

1.

Abnormal gait and posture: transient ischemic attacks(TIAs) , strokes, and Parkinson’s disease

COGNITIVE FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS

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•

•

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Ptosis (eyelid falldown); dropping of the upper eyelid over the globe—strokes of posterior inferior cerebellar artery; myasthenia gravis, palsy of CN III

Cranial VII (Facial nerve)—mixed nerve concerned with facial movement and sensation of taste 1. Loss of ability to taste 2. Decreased movement of facial muscles

3.

Inability to close eyes, flat nasolabial fold, paralysis of lower face, inability to wrinkle the forehead

4.

Eyelid weakness; paralysis of lower face; paralysis of upper motor neuron

5.

Pain, paralysis, sagging of facial muscles: affected side in Bell’s palsy

Cranial VIII (Acoustic)—composed of a cochlear division related to hearing and a vestibular division related to equilibrium (Phipps, 1998, p. 1909) • Decreased hearing or deafness: strokes of vertebralbasilar arteries or tumors of CN VIII Cranial IX(Glossopharyngeal) and cranial X (Vagus)— chief function of cranial nerve IX is sensory to the pharynx and taste to the posterior third of tongue; cranial nerve X is the chief motor nerve to the soft palatal, pharyngeal and laryngeal muscles (Phipps, 1998, p. 1909) 1. Dysphagia (difficulty swallowing) 2. Unilateral loss of gag reflex Cranial XI (Spinal accessory)—motor nerve that supplies the sternocleidomastoid muscle and upper part of trapezius muscles 1. Muscle weakness 2. Cortralateral hemiparesis: strokes affecting middle cerebral artery and internal artery Cranial XII (Hypoglossal) 1. Atrophy, fasciculations (twitches): LMN disease 2. Tongue deviation toward involved side of the body

SENSORY FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS • • •

Altered sensation occurs with variety of neurologic pathology Altered sense of position: lesions of posterior column of spinal cord Inability to discriminate fine touch: injury to posterior columns

MOTOR FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS • •

Muscle atrophy: LMNs disease Tremors (groups, large of muscle fibers)Parkinson’s disease (tremors at rest), multiple sclerosis (tremors observed in activity)

•

Fasciculations (single muscle fiber): disease or trauma to LMN, side effects of medications, fever, sodium deficiency, anemia Flaccidity (decreased muscle tone): disease or trauma to LMN and early stroke Spasticity (increased muscle tone): disease of corticospinal motor tract Muscle rigidity: disease of EP motor tract Cogwheel rigidity (muscular movement with small regular jerky movement; parkinson’s disease Muscle weakness-in arms, legs, hands: TIAs Hemiplegia-paralysis of half of body vertically Flaccid paralysis: strokes of anterior spinal artery, multiple sclerosis or myasthenia gravis Total loss of motor function: below level of injury Spasticity of muscle: incomplete cord injuries

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Positive Kernig’s sign-excessive pain when examiner attempts to straighten knees with client supine and knees and hips flexed

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Decorticate posturing (up)

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Decerebrate posturing (down)

CEREBELLAR FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS •

Ataxia (lack of coordination and clumsiness of movement, staggering, wide-based and unbalanced gait)

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Steppage gait (client drags or lifts foot high, then slaps foot onto floor; inability to walk on heels; disease of LMN Sensory ataxia (client walks on heels before bringing down toes and feet are held wide apart; gait worsens with eyes closed

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•

Romberg’s test (Positive)- With feet approximated, the patient stands with eyes open and then closed; if closing the eyes increases the unsteadiness, a loss of proprioceptive control is indicated

REFLEX

• •

1.

Parkinsonian gait (stooped over position while walking with shuffling gait with arms held close to the side)

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#Altered Level of consciousness

Hyperactive: reflexes Decreased reflexes Clonus of foot (Hyperactive, rhythmic dorsiflexion and plantar flexion of foot) Superficial reflexes (such as abdominal) and cremasteric reflex Positive Babinski reflex (dorsiflexion of big toe)

Consciousness Requires: 1. Arousal: alertness; dependent upon reticular activating system (RAS); system of neurons in thalamus and upper brain stem 2. Cognition: complex process, involving all mental activities; controlled by cerebral hemispheres

Process that affect LOC: a. Increased ICP b. Stroke, hematoma, intracranial hemorrhage c. Tumors d. Infections e. Demyelinating disorders

Systemic Conditions affecting LOC     

Special Neurologic Assessment

 •

Brudzinski’s sign (pain, resistance, flexion of hips and knees when head flexed to chest with client supine)

Hypoglycemia F/E imbalance Accumulated waste products from liver or renal failure Drugs affecting CNS: alcohol, analgesics, anesthetics Seizure activity: exhausts energy metabolites Level of Consciousness • Alert

• • • • •

Lethargic-very sleepy Obtunded Stuporous Coma Death

Client Assessment with Decreased LOC a.

Increased stimulation required to elicit response from client

b. c. d. e.

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More difficult to arouse; client agitated and confused when awakened Orientation changes: losses orientation to time first, then place, person Continuous stimulation required to maintain wakefulness Client has no response, even to painful stimulation

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Eyes may wander but cannot track objects Minimally conscious state: client aware of environment, can follow simple commands, indicates yes/no responses; make meaningful movements (blink, smile) Often results from severe head injury or global anoxia

Loss of Simultaneous Eye Movement Loss of normal reflex functioning: 1. Doll’s eye movement: eye movement in opposite direction of head rotation (normal function of brain stem) 2. Oculocephalic reflex: eye move upward with passive flexion of neck; downward with passive neck extension (normal function) 3. Oculovestibular response (cold caloric testing): instillation of cold water in ear canal cause nystagmus (lateral tonic deviation of eyes) toward stimulus (normal function)

Eye opening responses response to voice response to painful stimuli open eyes Best verbal response 5 4 3 2

Opens eyes spontaneously 3 Opens eyes in 2 Opens eye in 1 Does not

Oriented Confused Utters inappropriate words Incomprehensible words 1 None

B est motor response 6 5 3 2 1

1.

2.

3.

Obeys command Localizes pain 4 Withdraws with painful stimuli Flexion (Decorticate posturing) Extension (Decerebrate posturing None

Total 3-15 14 – no impairment 3 – compatible with brain death 7 – state of coma

1. 2.

a. b.

Client follows verbal commands Pushes away purposely from noxious stimuli

c.

Movements are more generalized and less purposeful (withdrawal, grimacing) Reflexive motor responses Flaccid with little or no motor response

COMA Irreversible coma - vegetative state •

•

Occurs with hemorrhage or infarction of pons, disorders of lower motor neurons or muscles

Permanent condition of complete unawareness of self and environment, death of cerebral hemispheres with continued function of brain stem and cerebellum Client does not respond meaningfully to environment but has sleep-wake cycles and retains ability to chew, swallow and cough

Cessation and irreversibility of all brain functions General criteria: a. Absent motor and reflex movements b. Apnea c. Fixed and dilated pupils d. No ocular responses to head turning and caloric stimulation e. Flat EEG

NURSING DIAGNOSIS • Ineffective airway clearance: limit suctioning to <10-15 seconds, hyperoxygenate • Risk for aspiration • Risk for impaired skin integrity: preventive measures, continual inspection • Impaired physical mobility: maintain functionality of joints, physical therapy • Risk for Imbalanced Nutrition: Less than body requirements • Anxiety (of family)

ICP 

Increased blood volume, increased brain volume, increased CSF volume



Normal pressure: 5-15 mmHg, with pressure tranducer with head elevated 30˚; 60-180 cmH20, water manometer with client lateral recumbent Sustained increases associated with: a. Cerebral edema b. Head trauma c. Tumors d. Abscesses e. Stroke f. Inflammation g. Hemorrhage



MOTOR FUNCTION ASSESSMENT

d. e.

Client is alert and fully aware of environment; intact cognitive abilities but unable to communicate through speech or movement because of blocked efferent pathways from brain Motor paralysis but cranial nerves may be intact allowing client to communicate through eye movement and blinking

Brain Death

GLASGOW RESPONSE 4

Locked-in syndrome



Factors • • • • • • • • •

that Increases ICP Hypercapnea, hypoxemia Cerebral vasodilating agents Valsalva maneuver; coughing or sneezing Body positioning (prone, neck flexion, extreme hip flexion) Isometric muscle contraction Emotional upset; noxious stimuli Arousal from sleep Clustering of activities Pain and agitation

ICP Cranial insult

2.

Tissue edema

Increased ICP

3.

Risk for infection: open head wounds and intracranial monitor device requires meticulous aseptic technique Anxiety (family)

Compression of blood vessels

Client with Seizure Disorder

Decreased cerebral blood flow Decreased oxygen with brain cell death Edema around necrotic tissue Increased ICP with brainstem and respiratory center compression

Epilepsy: any disorder characterized by recurrent seizures

Carbon dioxide accumulation Vasodilation

Pathophysiology:

Increased ICP

Seizures-alteration in consciousness, sensory and motor • Paroxysmal motor, sensory, or cognitive manifestations of spontaneous abnormal discharges from neurons in cerebral cortex • May involve all or part of brain consciousness, autonomic function, motor function and sensation

DEATH

pressure results to lack of oxygen and

blood supply Manifestations: • Decreasing level of sensorium-most sensitive, reliable and earliest indicator: due to cerebral hypoxia, interference with RAS function • Increasing BP, decreasing pulse • Pupillary changes (a reflection of tissue shifts • Cushing’s triad-increasing systolic pressure, widening pulse pressure and bradycardia (final compensatory mechanism to maintain CSF) • Papilledema-due to the compression of optic disc • Respiratory changes-dependent on site of pressure • Motor changes-dependent on site of pressure; usually starts contralaterally; then hemiplegia, decortication or decerebation depending on pressure on brain stem

Categorization of seizures:

Partial seizures: activation of part of one cerebral hemisphere a. Simple partial seizure: no altered consciousness, recurrent muscle contraction; motor portion of cortex affected

b.

Generalized seizures:  Involves both brain hemispheres; consciousness always impaired  Absence seizures (petit mal): characterized by sudden brief cessation of all motor activity, blank stare and unresponsiveness often with eyes fluttering Tonic-clonic seizures  Preceded by aura, sudden loss of consciousness  Tonic phase: rigid muscles, incontinence (as muscle contracts, bladder relax)  Clonic phase: altered contraction, relaxation, eyes roll back, froths at mouth  Post-ictal phase: unconscious and unresponsive to stimuli

Late signs: coma, apnea, unilateral pupil changes Medications for Increased ICP • Osmotic diuretics increases osmolarity of blood and draw fluid from edematous brain and tissue into vascular bed • Loop diuretics such as furosemide • Antipyretics or hypothermia blanket: used to control increases in cerebral metabolic rate • Anticonvulsants to manage seizure activity • Histamine H2 receptors to decrease risk of stress ulcers • Barbiturates: may be given as continuous infusion to induce coma and decrease metabolic demands of injured brain • Vasoactive medicine may be given to maintain blood pressure to cerebral perfusion Surgery-include removal of brain tumors, burr holes, insertion of drainage catheter or shunt to drain excessive CSF ICP monitoring • Continuous intracranial pressure monitor is used for continual assessment of ICP and to monitor effects of medical therapy and nursing interventions • Risk of infection exists with invasive procedure Nursing Diagnosis 1. Ineffective Tissue perfusion

Complex partial seizure: impaired consciousness; may engage in automatisms (repetitive nonpurposeful activity such as lip smacking, preceded by aura, originates in the temporal lobe)

State Epilepticus 1.

Continuous seizure activity, generally tonic-clonic type 2. Client at risk to develop hypoxia, acidosis, hypoglycemia, hyperthermia, exhaustion 3. Life threatening medical emergency requiring immediate treatment: a. Establish and maintain airway b. Diazepam (Valium) and Lorazepam (Ativan) intravenously at c. 50% Dextrose IV d. Phenytoin (Dilantin) IV-increase seizure threshold e. Pentobarbital-lessen nervous irritation Medications:

a. b. c. d. e.

Manage but do not cure seizures Raise seizure threshold Carbamezepine Phentoin Valproic acid

Key Interventions:

1. 2. 3.

Proper client from injury and maintaining airway Do not force anything into the client’s mouth Loosen clothing around neck

Nursing Diagnosis: 1. Risk for Ineffective airway clearance 2. Anxiety Interventions: 1. Assess for signs and symptoms of seizure activity such as report of aura or twitching of muscle groups 2. Have an oral airway oxygen and suction readily available 3. Stay with client to protect him from injury and observe seizure activity. If he is in bed, remove pillows, raise side rails, put bed on flat position. Loosen any restrictive clothing 4. After seizure, assess respiration and pulse. If they present and he is unresponsive turn him onto his side to keep his airway patent 5. Cover him with a blanket for warmth and privacy 6. Observe and document characteristics of the seizure

Client with Headache 1.

Dilate blood vessels Pressure on nerves 5.

Migraine headache: 1:4 household  Women 3x more than men: 3days a week  May be caused by: Light Noise Irregular eating and sleep Chocolate Strong smell Peanut butter Electrical impulse altered and triggers trigeminal nerve Trigeminal nerve=vasodilation and nerve irritation

6.

Cluster Headache  Excruciating pain  6 x more in men, 30 min to 2 hours Nerves irritated

May be due to benign or pathological condition

Pain signals

Pathophysiology: multiple pain sensitive structures within cranial vault, face, and scalp are stimulated and cause pain perception Types: Tension-characterized by sensation of tightness around head and may have specific localized painful areas; areas caused by sustained contraction of muscles and head and neck; precipitated by stress and anxiety Migraine (more common in women) recurring vascular headache often initiated by triggering event and accompanied by neurologic dysfunction; or increase release of sensory substances (e.g. serotonin); triggers include stress, fluctuating glucose levels, fatigue, hormones, bright lights Cluster (common in men) typically awakens client with unilateral pain around eye accompanied by rhinorrhea, lacrimation, flushing; attacks occur in clusters of 1-8 days for weeks

HEADACHE 1. 2.

Tension headache-90% ; noise, stress—sustained contraction of muscles Sinus Headache Virus, allergen, bacteria, temp Nerves in sinuses swell Headache e.g. brain freeze due to swallowing of cold substances rapidly

3.

Hang-over headache Alcohol blocks hormonal mechanisms Dehydration

4.

Wine headache Increases histamine/tyramine

Tension Headache Management: Pharmacological 1. Aspirin, Ibuprofen-suppress prostaglandin that dilates and sensitize nerve fibers 2. Acetaminophen-tension headache; works in CNS to reduce pain without effect on prostaglandin (safe for gastritis) 3. Triptans-anti-migraine; activates serotonin receptors decreasing inflammation of blood vessels 4. Botox (purified botulinum bacteria) small dosages allow it to be localized; paralyses muscles locally and is not absorbed into the blood stream (may cause nerve paralysis if given in large doses) 5. Indomethacin-for cluster headaches; with pain killers Nonpharmacological: 1. Biofeedback 2. Acupuncture 3. Massage 4. Yoga 5. Herbal remedies

HEAD INJURY    

Laceration Hematoma Contussion Bleeding Sources: 1. Scalp injury 2. Skull fracture 3. Brain injury

Risk factors: a. Motor vehicle accidents b. Elevated blood alcohol levels c. Greatest risk: male aged 15-30 and those over 75 Mechanism of trauma: 1. Acceleration injury: head struck by moving object

2. 3.

Deceleration injury: head hits stationary object Acceleration-deceleration (coupcountercoup phenomena) head hits objects and brain rebounds within skull

C.

Cerebral edema and Increasesd ICP

Skull fracture •

Diffuse axonal injury-most severe form of brain injury also called shearing injury

a.

Types of brain Injury: a. Open head injuries (dura) b. Closed head injuries –blunt trauma c. Concussions –caused by sudden blow to the head or rapid acceleration-deceleration  results in retrograde amnesia and loss of consciousness for 5 minutes  No break in skull or dura  May have headache, nausea or vomiting d. Contusions-cause more damage, damage to brain itself involve cortical bruising and laceration of vessels and brain tissues

b.

c.

Assessment: • Rhinorrhea: through nose • Otorrhea: through • May appear on x-ray • Hemotympanum: blood behind tympanic membrane (purple or dark color) Normal: pearly gray • Battle’s sign: blood over mastoid process • Raccoon eyes: bilateral periorbital ecchymosis • Glucose reagent strip: If positive indicates CSF

Complications of Brain Injury A. Post concussion syndrome: Manifestations:  Headache, dizziness  Nervousness, irritability  Changes in intelligence, poor concentrating, poor memory  Fatigability  Insomia Traumatic Brain Injury Epidural Subdural Intracerebral B.

Hematoma Formation: 1. Subdural hematoma (slower progression)veins, poor prognosis due to late diagnosis; occurs within 24-48 hours of injury in acute, 214 days in subacute; can occur up to several months in chronic

Manifestations: Acute • Progressive and marked depression of consciousness • Headache, drowsiness, agitation and confusion • Pupillary and motor changes Chronic • Increasing severe headache • Slow cerebration and drowsiness • Papilledema and ipsilateral pupil dilatation Systemic-Bilateral 2. Epidural (extradural) Hematoma

• • 3. •

Immediate loss of consciousness, lucid interval lasting for few minutes or hours; lapse into unconsciousness Severe, headache, seizures, vomiting, hemiparesis, fixed, dilated ipsilateral pupils

Intracerebral Hematoma Contained well-defined blood clot; usually at frontal and temporal lobes

Management: Craniotomy

break in continuity of skull usually resulting in brain trauma Linear: dura remains intact; subdural or epidural hematoma may occur underneath Comminuted and depressed skull fractures: increase risk for direct injury to brain tissue from contusion (bruise) and bone fragment: risk for infection Basilar: involves base of skull (softer) and usually involves extension of adjacent fractures

Interventions:

a. b. c.

Keep nasopharynx and external ear clean No blowing nose, coughing or hard sneezing Prophylactic antibiotic

Nursing Management for head injuries: Immediately following surgery: • Immobilize head and neck until cervical injury is ruled out • Avoid flexion: hyperextension and rotation of the neck • Jaw thrust maneuver Patent airway and support ventilatory function Document baseline neurological assessment After initial stabilization: • Monitor neurological status every hour until stable LOC, responsiveness Pupillary size, position, direct and consensual response Assess extraocular movements Note verbal and motor changes • Monitor for complications Hematoma formation Infection Acute hydrocephalus ARDS • • • • • •

Monitor temperature and maintain normothermia (decrease metabolism) Report high urine output (over 200 ml/hr for 2 consecutive hours) Monitor osmolality and serum electrolytes CBC ROM exercises Eye/ear care

• •

Nutrition-NGT (high glucose-brain functioning; protein-tissue repair) Elimination-laxatives, increase fiber

Craniotomy-surgical opening of the skull Craniectomy –permanent removal of the cranium to relieve pressure on the brain by providing space for expansion Nursing management Preoperative • Parenteral corticosteroids • Scalp preparation • Antiembolism stockings Postoperative 1. Neurological assessment 2. Head dressings:monitor for CSF leaks 3. Control ICP • Assess for signs of increasing ICP • Positioning to prevent increase in ICP  Supratentorial surgery-elevate head of bed 30 degrees  Infratentorial-keep flat, turn every 2 hours, but never onto the back (to prevent brain hernation)  Posterior fossa surgery-either side but never on the back  Bone flap-on the unoperated side

STROKE Stroke is a brain attack • …needing emergency management, including specific treatment and secondary and tertiary prevention Stroke is an emergency • …where virtually no allowances for worsening are tolerated Stroke is treatable • …optimally, through proven, affordable, culturally-acceptable and ethical means Stroke is preventable • …in implementable ways across all levels of society

Basic Location of Cerebral Aneurysm Cerebral embolus-moving Cerebral thrombus Cerebral hemorrhage Types of strokes •

Ischemic stroke-little blood flow 1. Thrombotic formation of a blood clot with coagulation the results in the narrowing of the lumen of a blood vessel with eventual occlusion 2. Embolic –occlusion of a cerebral artery by an embolus, resulting in necrosis and edema of the area supplied by the involved vessel

•

Hemorrhagic stroke-disrupted blood flow 1. Intracerebral hemorrhage stroke-bleeding within the brain caused by a rupture of vessels 2. Subarachnoid hemorrhagic stroke-cause by aneurysm or AV malformation

Development of CVA

1. 2.

3. 4.

Transient Ischemic attack-brief episodes of neurologic manifestations which clear completely in less than 24 hours Reversible ischemic neurologic deficit-neurologic deficits remain after 24 hours but leaves no residual signs and symptoms after days to weeks Stroke in-evolution-progressing stroke which develops over a period of hours or days; manifestations don’t resolve and leave residual neurologic effects Completed stroke- when neurologic deficits remain unchanged over 2-3 day period

Risk Factors • Prior ischemic episodes •Cardiac disease •DM •Atherosclerotic diseasae •Hypertension, hypercholesterolemia •Polycythemia •Smoking •Oral contraceptives •Emotional stress •Obesity •Family history of stroke •Age Warning signs that may precede CVA •Paresthesia •Transient loss of speech •Hemiplegia •Severe occipital or nuchal headaches •Vertigo or syncope •Motor or sensory disturbances (tingling transient paralysis) •Epistaxis SPECIFIC DEFICITS Dependent upon area damaged •Hemiplegia •Aphasia sensory/receptive-Wernick’s aphasia motor/expressive-Broca’s aphasia (able to understand the stimuli but cannot express •Global aphasia Agnosia Dysarthria Incontinence Horner’s syndrome-decrease lacrimation Unilateral neglect Emotional or Behavioral Reactions: •Severe mood swings •Social withdrawal •Inappropriate sexual behavior •Outbursts of frustration and/or anger •Regression to an earlier behavior Right brain damage

•Paralyzed left side •Spatial-perceptual deficits •Tend to deny or minimize problems •Impaired judgment •Impaired time concepts •Short term span

Left brain damage

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

cautious

Middle cerebral artery Involvement •Contralateral paralysis •Contralateral anesthesia, loss of proprioception, fine touch, localization •Aphasia •Neglect of opposite side •Homonymous hemianopia-loss of vision for one half of the visual field Diagnostic procedures  CT scan-determine if vascular or nonvascular lesions  Angiography  MRI  Laboratory (CBC, PT, PTT)-not definitive to conform diagnosis Medical management  Decreased ICP  BP management  Fluid volume management  Tissue plasminogen activator-must be given within 3 hours of onset of manifestations and will dissolve clot; recombinant altephase (Activase rt-pa)  Antithrombotic (aspirin, clipyridamole)-prevent platelet aggregation  Anticoagulant (heparin, clexane)  Steroids or osmotic, diuretics  Antihypertensive and diuretics Nursing management  Hourly neurological assessment  Monitor and prevent intracranial hypertension

•Positioning -

bed rest: keep mainly on unaffected side use of pillows to support to prevent flexion deformity, thrombus formation external hip rotation assist in progressive activity (mobility) Progressive self-care (ADL)

•Prevention of injury eyes-normal saline, artificial tears, eye patch side rails up decubitus ulcer prevention/management Oral mucosa care •Nutrition/prevention of aspiration Communication Others:  Reorientation  Minimize environmental stimuli  Emotional support  Rehabilitative •Discharge care Ways to prevent recurrence  dietary modification  Stress reduction  Smoking cessation  Exercise program  Drug compliance Residual deficits and balancing realistic expectation Special methods of feeding Ensure continuity of care and emotional support

SPINAL CORD INJURY Manifestations: Subjective •Loss of sensation below level of injury •Inability to move Objectivity A. Early symptoms of spinal shock •Absence of reflexes below level of lesion •Flaccid paralysis below level of injury •Hypotonia results in bowel and bladder distention •Inability to perspire in affected parts •Hypotension B. Later symptoms of spinal cord injury •Reflex hyperexcitability •State of diminished reflex hyperexcitability below site in all instances of cord damage following hyperreflexia •In total cord damage-loss of motor and sensory function is permanent •Sacral region-atonic bladder and bowel with impairment of sphincter control •Lumbar region- spastic bladder and loss of bladder and anal sphincter control •Thoracic-trunk below the diaphragm •Cervical-from neck down, if above C4 respirations and depressed •In partial cord damage, depends on the type of neurons affected (spastic vs. flaccid) Clinical manifestations: •Paralysis of muscles of respiration •Bradycardia •Hypotension •Urinary retention •Hypomotility •Muscle atrophy •Poikilothermia-abnormality in sensing change in temperature

-

MUSCLE FUNCTION AFTER SPINAL CORD INJURY (((log-rolling) Spinal Cord Injury Cervical, above C4 C5 C6-C7

Thoracic Lumbo-sacral

Muscle Functioning remaining None Neck, scapular elevation Neck, some chest movement, some arm movement Neck, arms (full), some chest Neck, arms, chest, turnk

Laminectomy

Muscle Function Loss All including respiration Arm, chest, all below chest Some arm, fingers, some chest movement all below chest Trunk, all below chest Legs

Autonomic dysreflexia (after spinal shock resolves)

Exaggerated autonomic response to stimuli: such as distended bladder or bowel (e.g. pain)



•

Severe hypertension

•

Headache

•

Flushed skin

•

Diaphoresis

•

Nasal Congestion

Management 1.

Place in high-Fowler’s position

2.

Ensure patency of urinary drainage and assess for infection.

3.

Eliminate other potential stimuli

4.

Notify physician: administer prescribed antihypertensive

Parkinson’s Disease (fourth common neurodegenerative disease) •

Degeneration of dopamine-providing cells in the substantia nigra, which leads to degeneration of neurons in the basal ganglia; usually develops after 60 age

•

Associated with decreased levels of dopamine due to destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia of the brain (Smelzer & Bare, 2004, p. 1979)

•

Imbalance between dopamine and acetylcholine

Three cardinal features: 1. Tremors at rest •

Nursing Diagnosis 1.

Impaired gas exchange related to muscle fatigue and retained secretions.

2.

Decreased cardiac output r/t venous pooling and immobility

3.

Impaired skin integrity r/t immobility and poor tissue perfusion

4.

Constipation r/t the injury, inadequate fluid intake, diet low in roughage and immobility

5.

Urinary retention

6.

Impaired physical mobility

7.

Risk for autonomic dysreflexia r/t reflex stimulation of SNS

8.

Altered nutrition less than body requirements r/t increased metabolic demand

9.

Sexual dysfunction r/t inability to achieve erection or perceive pelvic sensations

Medical Management 

Immoblization—Gardner –well tongs, halo external fixation



Maintenance of heart rate (Atropine) and BP (dopamine) vasopressors

•

e.g. rhythmic, slow turning motion (pronation-supination) of the forearm and the hand and a motion of the thumb against the fingers as if rolling a pill tremor is present while at rest, increases when the patient is walking, concentrating, feeling anxious (Smeltzer & Bare, 2004, p. 1980).

2.

Rigidity-resistance to passive limb movement

3.

Bradykinesia-most common features; patients take longer to complete most activities and have difficulty initiating movement

Clinical Manifestations: •

Generalized feelings of stiffness

•

Mild, diffuse muscular pain

•

Hand tremor at rest (pill rolling)

•

Akinesia

•

Gait changes –shuffling gait

•

Characteristic stance-stooped posture

•

Masklike-facial expression

•

Speech pattern-slow, low volume monotonous in tone with poor articulation



Methylprednisolone therapy



Insertion of NGT

•

Involuntary drooling



Intubation, if needed

•

Decreased lacrimation; constipation, incontinence



Indwelling urinary catheter

•

Heat intolerance; excessive perspiration



Stress ulcer prophylaxis (Proton-pump inhibitos, H2 blockers)

•

Lack of spontaneous swallowing



Physical therapy

Medical Management

•

Levodopa-Carbidopa T-synthetic precursor of dopamine for basal ganglia (Sinemet)

•

Anticholinergic-to control symptoms (Cogentin, Artane, Symmetrel); anticholinergics drugs act at central sites to inhibit cerebral motor impulses that cause rigidity of themusculature

•

•

MAOI-Bomcriptine; inhibit breakdown of dopamine

•

•

Physiotherapy-reduces rigidity of muscles and prevents contractures

•

•

Believed to be due to reduced acetylcholine receptors due to destruction and blockage attributed to autoimmune process An autoimmune disorder, characterized by varying degrees of weakness of the voluntary muscles (Smeltzer & Bare, 2004, p. 1956) Highest in young adult females.

Manifestations

Subjective:  Extreme muscle weakness, worsens as the muscle is used but disappears with rest

Surgical intervention-to destroy globus pallidus (to relieve rigidity) and/or thalamus (relieve tremors)

Nursing Management •

Provide safe environment

•

Nutrition



•

•

Small frequent meals for easy mastication



Adequate intake of roughage to prevent constipation



Encourage diet rich in nutrient-dense foods such as fruits, vegetables, whole grains

Limit postural activities



Maintain gait as normal as possible: may utilize cane or wheel chair



Encourage daily physical therapy to limit rigidity and prevent contractions



Medication compliance; report side effects

Avoid rushing client as he is unable to work under pressure

•

Assist client in setting achievable goals to improve self-esteem

•

Total body function support in advanced stages (respiratory elimination)

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

Diplopia (double vision)



Dysarthria



Myasthenia smile (nasal smile)



Strabismus

Myasthenia gravis is purely a motor disorder with NO effect on sensation or coordination (Smeltzer & Bare, 2004, p. 1956)

Diagnostic Test 

Neostigmine (Prostigmine)—subcutaneous or IV administration of tensilon (prevents enzymatic breakdown of Ach) to provided relief of symptoms



The thymus gland, which is a site of acetylcholine receptor antibody production is enlarged in myasthenia gravis (Smeltzer & Bare, 2004)

Medical Management  Pharmacologic -

Acetylcholinesterase blockers

-

Corticosteroids to suppress immunity



Plasmapheresis -



X-ray or surgical removal of thymus (thymectomy)

Myasthenic Crisis •

Sudden inability to swallow or maintain respirations due to weakness of the muscles of respiration; undermedication

•

Exacerbation of the disease process characterized by severe generalized muscle weakness and respiratory and bulbar weakness that may result in respiratory failure (Smeltzer & Bare, 2004, p.1957)

Myasthenia Gravis •



Note:

Positioning and activity 

Dysphagia

Objective:  Ptosis of the eyelid (both eyes)

Small bite pieces of food to prevent choking





Cholinergic Crisis •

Overdose of anticholinergic drugs

•

May mimic the symptoms of exacerbation

Note: Differentiation of myasthenic crisis and cholinergic crisis can be achieved with the edrophonium chloride (Tensilon) Test. The patient with myasthenic crisis improves immediately following administration, while patient with cholinergic crisis may experience no improvement or deteriorate (Smeltzer & Bare, 2004)

Guillain-Barre Syndrome •

Immunologic status often follows respiratory or GIT infection, viral immunization, trauma or surgery

•

An autoimmune attack of the peripheral nerve myelin (Smeltzer & Bare, 2004).

•

Areas of demyelination in the motor cells of the spinal cord and medulla (ascending loss) vs. ALS (descending)

•

Seen in adults 20-50 years

•

After initial and plateau periods recovery in 1 year sometimes with residual deficits, other dies of complications

ALS- common in males

Manifestations begins with muscle weakness and diminished reflexes of the lower extremities Subjective:  Generalized weakness 

Paresthesia



Diplopia

Objective  Ascending paralysis within the body usually 24-72 hours 

Respiratory paralysis



Hypertension, tachycardia and low grade fever



Incontinence

Medical Management 1.

Steroids

2.

Plasmapheresis

3.

Support of vital function

Nursing Management: Supportive care 1.

Respiratory management

2.

Nutritional management

3.

Prevent complications

4.

Emotional support

Client with Multiple Sclerosis 1.

Believed to be autoimmune response to prior viral infection

2.

Inflammation destroys myelin leading to axon dysfunction; neurons in spinal cord, brain stem, cerebrum, cerebellum and optic nerve affected

3.

Stressors trigger multiple sclerosis—febrile states, pregnancy, physical exertion and fatigue and these can trigger relapses

4.

Incidence is highest in young adults (20-40); onset between 20-50; females more than males

Manifestations 1.

Fatigue

2.

Optic nerve involvement: blurred vision, haziness

3.

Brain stem involvement: nystagmus, dysarthria (scanning speech); cognitive dysfunction, vertigo, deafness

4.

Weakness, numbness in legs, spastic paresis, bladder and bowel dysfunction

5.

Cerebellar involvement: nystagmus , ataxia, hypotonia

6.

Blindness

Meningitis •

Inflammation of pia matter, arachnoid and subarachnoid space

•

Spreads rapidly through CNS because of circulation of CSF around brain and spinal cord

•

May be bacterial, viral, fungal, parasitic in origin

•

Infection enters CNS though invasive procedure or through bloodstream, secondary to another infection in body

Bacterial Meningitis • Causative organism: Neisseria meningitides, Streptococcus pneumonia, Haemophilus influenza, Escherichia coli •

Manifestations a.

Fever, chills

b.

Headache, back and abdominal pain

c.

Nausea and vomiting

d.

Meningeal irritation:

4.

Manifestations depend on rate of onset: progressive cognitive dysfunction, gait disruptions, urinary incontinence



Nuchal rigidity (stiff neck)-early sign



Positive Kernig’s sign

•

Visual changes



Positive Brudzinski’s sign-when the patient’s neck is flexed, flexion of the knees and hips is produced

•

Increase in head size

•

Increase ICP



Photophobia –extreme sensitivity to light

e.

Meningococcal meningitis: rapidly spreading petechial rash of skin and mucous membrane

f.

Increased ICP: decreased LOC, papilledema – edema of optic disc due to increased ICP

Treatment/Management 1.

Diuretics

2.

Surgery

3.

Protect from injury from altered LOC and immobility

Viral Meningitis •

Less severe, benign course with short duration, intense headache with malaise, nausea, vomiting, lethargy, signs of meningeal irritation

Encephalitis 1. 2.

Acute inflammation of parenchyma of brain or spinal cord Usually caused by virus

Medications 1.

Meningitis: immediate treatment of effective antibodies for 7-21 days according to culture results; dexamethasone to suppress inflammation

Skeletal muscle •

Attach to the skeleton

•

Permits voluntary movements

•

Maintain posture

•

Generates heat

•

Innervated by the somatic nervous system

•

Produce movement by contraction

•

Sarcomeres-functional unit of striated muscle

Dilantin—Increase seizure threshold

Health Promotion 1.

Vaccinations for meningococcal, pneumococcal, haemophilus meningitis

2.

Prophylactic rifampins for persons exposed to meningococcal meningitis

3.

Mosquito control

4.

Prompt diagnosis

5.

Asepsis care for clients with open head injury or neurosurgery

Hydrocephalus

Basic Principles of skeletal muscle action 1. Motor unit should be stimulated to contract, absence of impulse conduction leads to paralysis 2.

Muscles are attached to at least 2 bones; with each contraction, muscle’s insertion bone moves and the muscle origin bone remains stationary

3.

Bone serve as levers; joint as fulcrums

Fractures -

Break in the continuity of bone

Classification: 

Closed-no break in the skin



Open-

Common Cause: 1. Noncommunicating obstruction in CSF drainage from ventricular system



Complete-involves break across the entire cross-section of the bone and is frequently displaced

2.

Communicating: CSF is not effectively reabsorbed through arachnoid villi



Incomplete e.g. greenstick, the break occurs through only part of the crosssection of the bone

3.

Normal pressure hydrocephalus: occurs in persons>60 in which ventricles enlarge causing cerebral tissue compression



Displaced



Comminuted-several bone fragments



Impacted or compression

•

Increase in volume of CSF within ventricular system, which becomes dilated



Complicated-accompanied by infection



Pathologic-systemic, loss of bone density

Clinical Manifestations

1.

Purposes: Immobilization

2.

Prevention or correction of deformity

•

Deformity

3.

Maintenance support and protection to realign bone

•

Swelling

4.

Promotion of healing which allows early weight bearing

•

Bruising

•

Muscle spasm

•

Tenderness

•

Pain

•

Impaired sensation

•

Loss of normal function

•

Crepitus- grating sensation resulting from rubbing of bone fragments against each other

Nursing Management: CAST Precast application Care- factual and sensory information -

•

Abnormal mobility of affected part

•

Hypovolemic shock

Intracasting Postcasting Drying 24-48 hours -

Proper handling

-

Watch for neurovascular complications

-

Watch for infection

-

Watch for cast syndrome (occurs with body casts)

Vasogenic shock-due to severe pain

Surgical/Medical Management  Open-reduction-alignment during surgery 

Internal fixation device placement: use of screws, wires, nails or rods



Closed reduction



Traction application



Management of shock



Prolonged nausea and vomiting



Abdominal distention and pain

Cast syndrome-psychological (claustrophobic reaction) and physiologic (superior mesenteric artery syndrome) responses to confinement in body cast (Smeltzer & Bare, 2004) -

Watch for: wet-spots-drainage: hot spotstissue infection or necrosis under casts

-

Elevated injured extremity especially for the first 24-48 hours

-

Prevents disuse syndrome

Nursing Management for Fractures 1.

Contraindications

•

Exercise joints before and after injured site

•

Isometric exercises, gluteal setting, abdominal tightening and deep breathing exercises

•

Skin care

•

Elimination

•

Nutrition- Vit C (absorption of calcium)

Assess neurovascular status (6 P’s) ulselessness allor ain aresthesia oikilothermia aresia/paralysis

2.

Assess skin

3.

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

4.

Analgesics-Opioid analgesics

5.

Rehabilitation

Cast Application

Cast care 

Keep cast dry; use plastic when bathing



Do not use powder or insert objects inside cast



Use of slings/crutches to enhance comfort safety and ambulation



Reportable conditions: -

Increased swelling

-

Tingling or burning sensation

-

Inability to move muscle around cast

-

Foul odor inside or around the edge

Principles of Effective Traction  Traction must be continuous to be effective in reducing and immobilizing fractures



Skeletal traction is never interrupted



Weights are not removed unless intermittent traction is prescribed



Any factor that might reduce the effective pull or alter its resultant line of pull must be eliminated:

Therapeutic Traction -

Pulling force

Types: 1. Skin 2.

Skeletal

3.

Cervical

4.

Pelvic

5.

Buck’s traction (unilateral or bilateral) is skin traction to the lower leg

6.

Russel’s – one leg is higher than the other

Techniques: 1. Running (Straight) applies the pulling force in a straight line with body part resting on bed 2.

Suspension (Balanced)-supports the affected extremity off the bed and allows for some patient movement without disruption of the line of pull

3.

Continuous intermittent

-

Patient must be in good body alignment in the center of the bed when traction is applied

-

Ropes must be unobstructed

-

Weights must hang free and not rest on the bed or floor

-

Knots in the rope or the footplate must not touch the pulley or the foot of the bed

-

(Smeltzer & Bare, 2004, p. 2026)

Nursing Care of Clients with Braces or Splints 1.

Check body and equipment alignment

2.

Keep equipment in good condition

3.

Examine integumentary integrity

Use of Cane 1.

Ascertain client capability to bear weight

2.

Ensure strength of upper extremity opposite lower

Care of Client 1. Know the purpose and contraindicated movements 2.

Pin site care-goal is avoid infection and development of osteomyelitis; site is covered with a sterile dressing (Smeltzer & Bare, 2004, p. 2028)

3.

Ropes and pulley should hang free

4.

Monitor color, warmth, movement and sensation of extremity distal to the traction every 4-8 hours ( neurovascular check)

5.

Devices such as trapeze, fracture pins

6.

Immobility problems (thrombophlebitis, diversional therapies , among others)



After traction: Gradually assume sitting position

extremity 3.

Ensure proper length of cane 

Highest point approximately at level of greater trochanter



Lack of proprioception response initially



30 degrees flexion of elbow



Joints may be unstable; may feel faint or weak for a while



Tip of the cane 15 cm (6 inches) lateral to the base of the fifth toe (Smeltzer & Bare, 2004, p. 174)

4.

5.

Ensure proper techniques

2.

Opposite affected extremity



Affected extremity cane simultaneously



Out of 100 types of with unknown cause



Should be close to the body



Common types:

Observe for incorrect use 

Leaning the body over the cane



Shortening the stride of the unaffected side



Persistence of abnormal gait



Strength of upper torso



Psychological fitness

4.

5.

Axillary bars 5 cm (2 inches below axilla), 15 cm (6 inches infront and lateral) tripod position

Assist in use of proper technique Four point- R crutch, L foot, LC, RF



Two-point-R crutch with L foot, then LC with RF



Three point-advance both crutches and weak extremity, then follow good foot



Swing to gait-advance crutches then swing feet to the level of the crutches



Swing through gait-advance crutches then swing through the crutches

Incorrect position 

Walking on ball of foot



Hunching shoulders



Looking downward



Hiking hips (common in amputees)



Bearing weight under arms may cause brachial plexus damage



Lifting crutches while still bearing down on them

Evaluate client’s response

Arthritis

Inflammatory –RA and SLE

2.

Non-inflammatory –degenerative joint disease

3.

Gout-crystal-produce disease from high protein ingestion

wear out or repair less effective; localized; NO synovial membrane swelling

Ensure proper fit



1.

Osteoarthritis  Autosomal recessive trait causing cartilages to

Ensure readiness of client



3.

Disease involving degeneration and or inflammation of joints and surrounding structures



Crutch Nursing care 1.



o

Wear and tear of joints

o

Obesity; joint trauma

o

Aging: 55 years old and above

o

Degeneration and atrophy of the cartilage and calcification of ligaments

o

Primarily affects weight-bearing joints, spine and hands



Degeneration of cartilages into the bony spur



Formation of subchondral osteophyte



Secondary synovitis (late manifestation)-pain and swelling with joint movement

Manifestations:  Joint stiffness 

Pain after exercise; pain with movement



Heberden’s (distal) and Bouchard’s (proximal) nodes



Decreased ROM



Crepitus

Medical Management  Steroids 

Antiinflammatory



Analgesics-salicylates and NSAIDs



Physiotherapy/Exercise



Surgery-replacement of mobility (knee and hips common)

Rheumatoid Arthritis



Systemic with synovial membrane inflammation with blood, fibrin, and coagulation deposits

bone slips over another and eliminates the joint space (Smeltzer & Bare, 2004, p. 1621)



Unknown cause: hereditary, autoimmune psychophysiologic factors, 25-55 years old

Gouty Arthritis



Exacerbations linked to physical and emotional stress



Inflammatory changes in the connective tissue



Mono-articular (one joint)



Hyperuricemia; 40-50 years old

Pathophysiology: Symmetrical joints

1.

Genetic increase in purine metabolism and production

2.

Ingestion of excessive alcohol or high purine diet

Synovial lining of joints become inflamed Pathophysiology:

Synovitis Increased fluid with pannus Pannus destroys cartilage and invade joint capsule Replaced by fibrous connective tissues

Uric acid-major by product of protein and nucleic acid metabolism Tendency to crystallize especially with dehydration, diuretics use and increased Tubular resorption to the systemic circulation

Affects tendons and ligaments Cause joint subluxation, bony ankylosis and consolidation of joints

Deposited in connective tissues and joints (esp. great toe) Release of lysosomal enzymes

Swelling, deformities Pain Manifestations: Subjective  Fatigue, malaise, anorexia 

Joint pain, stiffness after periods of inactivity especially a.m

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Paresthesia (destruction of nerve involved)

Objective  Joint inflammation and deformity 

Swan neck and Boutinniere deformities; ulnar drift, joint subluxation

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Increased ESR, low grade fever , positive rheumatoid factor

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Anemia, weight loss

Medical Management  Coticosteroids, anti-inflammatory, analgesics, immune suppressive drugs 

Plasmapheresis

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Antimalarial drugs—destroys autoimmune antibodies

 Note:

Inflammation Joint degeneration and disability and tophaceous (white in color) deposits in the joints May cause renal tubular damage leading to renal stones and failure Note:

Attacks of gout appear to be related to sudden increases or decreases of serum uric acid levels. When the urate crystals precipitate within a joint, an inflammatory response occurs and an attack of gout begins. With repeated attacks, accumulation of sodium urate crystals, called tophi, are deposited in peripheral areas of the body, such as great toe, the hands, and the ear (Smeltzer & Bare, 2004, p. 1630). Manifestations: Tight/reddened skin around inflamed joint, edema Pain

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Increase temperature

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Hyperuricemia> 7.5 mg/dl

Management of Gout 1. Decrease protein in diet 2.

Weight control and decrease alcohol ingestion

3.

Increase fluids to 3000 ml/day (the more dehydration, more crystallization)

4.

Joint rest

5.

Allupurinol/Probenecid, Colechicine

Cytotoxic drugs

Deformities of the hands and feet are common in RA. The deformity may be caused by misalignment resulting from swelling, progressive joint destruction, or the subluxation (partial dislocation) that occurs when

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High Purine foods

1.

Poultry

2.

Organ meats

3.

Meat extracts

4.

Seafoods, sardines, anchovies, shrimp herring

5.

Asparagus, spinach, mushroom

Surgical intervention 1. Arthrodesis-surgical fusion of a joint to render a joint immobile but decreases pain and increases strength 2.

Osteotomy-transection of a bone to correct a deformity or misalignment

3.

Resection-for partial removal of a degenerated bone (wrist and foot)

4.

Replacement arthroplasty-joint replacement

Assistive devices: 1. Eating utensils 2.

Braces

3.

Walkers

4.

Cane-single, quad

Therapies 1. Diversion 2.

Exercise, ROM, quadriceps exercise

3.

TENS

4.

Cold and warm pack 30 minutes before activities

5.

Whirl pool bath

6.

Balance rest and activity

7.

Assistive devices, elevated chair or toilet to 3-4 inches

Nursing Diagnosis • Chronic pain related to joint degeneration •

Impaired physical activity r/t restricted mobilization

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Activity intolerance

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Self-care deficit

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Body image disturbance r/t visible body changes/deformities/misalignment

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Knowledge deficit

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Sleep pattern disturbance