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Ronnie V. Mayo, MD, RN, MSN
A. Central Nervous System B. Peripheral Nervous System C. Autonomic Nervous System
Central Nervous System
A. Brain - Cerebral Hemispheres and Diencephalon - Brainstem - Cerebellum B. Spinal Cord
Peripheral Nervous System
A. Cranial Nerves
B. Peripheral Nerves
31 pairs ( cervical, thoracic, lumbar, sacral, coccygeal)
Autonomic Nervous System Sympathetic Parasympathetic .
Neurons Dendrites Cell body Axon .
Nerve Structure .
Skull Frontal View Location for placement of ICP catheters Anterior to coronal suture & off midline (Saggital sinus underneath) Midline Frontal .
Skull Lateral View Frontal Temporal Parietal Occipital Coronal suture Frontal Parietal Sutures Separation between bones Underlying coronal suture is motor strip Temporal Occipital .
Dura Mater Tough outer layer.meningeal forms compartments . inelastic.periosteum brain . fibrous membrane Double layered Attaches to skull .
Dura Mater Compartments Right & left side Supratentorial (contains cerebral hemispheres) Infratentorial (posterior fossa – contains brain stem & cerebellum) .
Arachnoid Membrane Middle layer Delicate avascular membrane Forms the subarachnoid space and cisterns .
Arachnoid Membrane Contains CSF (cerebral spinal fluid) in space below Arachnoid granulations project into venous sinus Clinical relevance Subarachnoid hemorrhage (SAH) .
Pia Mater Innermost layer adherent to brain Mesh-like. vascular .
Spaces between the coverings Epidural Potential space between the dura and skull Bleeding occurs from the middle meningeal artery .
Spaces between the coverings Subdural Potential space between the dura and arachnoid Bleeding occurs from injury to bridging veins Placement of subdural catheters .
Spaces between the coverings Subarachnoid Space between the arachnoid and pia mater Contains major arterial vessels Bleeding may be due to rupture of a vessel .
Arterial Brain uses 15-20% of cardiac output Blood supply into brain Anterior circulation Carotid arteries Common to internal Posterior circulation – Vertebral arteries Internal carotid Common carotid .Cerebral Circulation .
Cerebral Circulation .Arterial Carotid Stenosis (narrowing) Treated by carotid endarterectomy Use carotid shunt .
Arterial Circulation Circle of Willis Interconnection of arteries that supply blood to cerebral hemispheres Posterior circulation Supplies blood to brainstem .
Venous Drainage Occurs through the bridging veins Brain .dural sinus .through arachnoid .
Licox) Obstruction of venous pathways .Venous Drainage Clinical Observations About 80% blood volume is venous Avoid sagittal sinus with placement of Monitoring (ICP.ICP .
Cerebral Lobes Frontal Parietal Temporal Occipital Parietal Occipital Frontal Temporal .
Frontal Lobe Motor function Contraction and synchronization Cognitive functions Judgment Uniqueness of personality Reasoning Broca’s speech center – ability to talk Long term memory .
Parietal Lobe Sensory interpretation Touch Temperature Taste .
shape.Occipital Lobe Visual brain Appreciation of size. and color .
Temporal Lobe Sensation and interpretation of sounds Interpret sense of smell Control behavior patterns .
Ventricular System Fluid filled cavities deep in cerebrum filled with Cerebrospinal Fluid (CSF) .
Ventricular System Four ventricles 2 Lateral Location for ventricular catheters Third Fourth Connected by Foramen of Monro Landmark used to zero transducers & EDV’s .
Ventricular System Lateral View AP View .
Ventricular System Choroid Plexus Very vascular Found throughout ventricular system but mostly in lateral 500cc CSF produced daily Approx 20cc produced hourly 150cc in the system at any time .
. Travels around spinal cord & exits thru Arachnoid Granulations. Exits through Foramen of Magendie & Foramen of Luschke.CSF Flow-path Lateral ventricles thru Foramen of Monro to 3rd ventricle thru aqueduct of Sylvius to 4th ventricle.
shunt (VP or LP) . lumbar drain.Hydrocephalus – excess CSF Communicating Flows thru system Usually a decrease reabsorption of CSF (blockage in arachnoid villi due trauma or SAH) Ventriculostomy.
Hydrocephalus Non-communicating CSF unable to flow thru the system Congenital Obstruction Cysts VP shunt .
Midbrain.Diencephalon. Brainstem and Cerebellum .
Diencephalon Thalamus Process incoming sensory information before distribution to the somatosensory cortex Process motor information from the cerebral cortex and cerebellum and projects its analysis back to the motor cortex Contributes to the concentrating ability by filtering out distracting sensory input Contributes to emotional component of sensations (pleasant or unpleasant) .
peristalsis. BP. (heartbeat. and gland secretions) Secretes neuropeptides (TRH and LH-RH) Produces ADH and oxytocin Contains appetite center. automatic functions.Diencephalon Hypothalamus forms a crucial part of the neural path by which emotions and other cerebral functions can alter vital. satiety center and temperature regulating center Maintains waking state (arousal or alerting neural pathway) .
and various regions of the cerebral cortex Reflex centers for cranial nerves III and IV Pineal body .Midbrain Located between pons. diencephalon and cerebrum Integrates and analyzes sensory input from the ears. eyes.
respiratory reflexes.Brainstem Medulla Conducts impulses between the cord and brain Contains important reflex centers for heart. and swallowing . vomiting. blood vessel diameter. coughing.
and VIII. VII. Contains pneumotaxic center . VI.Brainstem Pons Conducts impulses between the cord and various parts of the brain Contains reflex centers for cranial nerves V.
Cerebellum Exerts synergic control over the skeletal muscles producing smooth. steady. and precise movements Coordinates skeletal muscle contractions and play an essential part in producing normal postures and maintaining equilibrium .
Spinal Cord Cervical Thoracic Lumbar Sacral Spinal cord .
Spinal Cord From foramen of magnum to the 1st lumbar vertebra Inner core consist of gray matter. shaped like a three dimensional H Long columns of white matter surround the cord’s inner core of gray matter (composed of numerous sensory and motor tracts). Right and left anterior columns Lateral and posterior columns .
Spinal cord .
Spinal Cord Functions Sensory tracts conduct impulses up cord to brain Motor tracts conduct impulses down cord from brain Gray matter of cord contains reflex centers for all spinal cord reflexes .
thoracic. sacral. Cranial Nerves 12 pairs B. lumbar. Peripheral Nerves 31 pairs ( cervical.Peripheral Nervous System A. coccygeal) .
Cranial Nerves Cranial I and II – direct extensions of receptor organ Cranial Nerve III. VI. XI. VII. XII . IV – midbrain Cranial Nerve V. VIII – pons Cranial Nerve IX.medulla . X.
and glandular tissues Consist of 2 divisions: Sympathetic nervous system and Parasympathetic nervous system . smooth muscles.Autonomic Nervous System Conducts impulses from the brainstem or cord out to visceral effectors: cardiac muscles.
Autonomic Nervous System Sympathetic Nervous System Adrenergic fibers secrete norepinephrine Influences smooth muscle of blood vessels and hairs and sweat glands Under conditions of stress. . sympathetic impulses to the visceral effectors usually increase greatly and dominate over parasympathetic impulses.
Autonomic Nervous System Parasympathetic Nervous System Cholinergic fibers secrete acetylcholine Influences digestive tract and smooth muscles to promote digestive gland secretion. and defecation Influences heart to decrease rate and strengthen contractility Vagus nerve is the most significant parasympathetic nerve . peristalsis.
Diseases of the Nervous System .
violence.Head Injury Includes Scalp injury Skull Brain Traumatic Brain Injury Most serious form of head injury Motor vehicles. under 5. over 75 Best approach is prevention . falls 15 to 24 years of age.
Pathophysiology Two Forms Primary Initial damage to the brain Secondary Evolves over the ensuing hours and days after the initial injury Due to brain swelling and ongoing bleeding .
contusion. Potential portals for organisms Irrigate before suturing . or hematoma beneath the layers of the scalp (subgaleal hematoma) Diagnosis: physical exam. palpation. inspection.SCALP INJURY Scalp trauma bleeds profusely when injured Abrasion. laceration.
or basilar. May be open – scalp laceration. tear in the dura May be closed – dura is intact .SKULL FRACTURES Break in the continuity of the skull With or without damage to the brain Linear. depressed. comminuted.
SKULL FRACTURE DIAGNOSIS Skull Series Cranial CT-Scan Cranial MRI .
surgery may be delayed for 3 to 6 months Penetrating wounds require surgical debridement Antibiotic treatment .MEDICAL MANAGEMENT Conservative Management For non-depressed skull fracture Surgical Management Contaminated or deforming fractures If significant cerebral edema is present.
TRAUMATIC BRAIN INJURY (TBI) Rigid close compartment Do not allow expansion Any bleeding or swelling increases volume – increases ICP Increase ICP – downward and lateral displacement of the brain Displacement – restriction of blood flow – oxygen delivery Brain becomes anoxic – irreversible brain damage .
TBI: CLINICAL MANIFESTATIONS Altered level of consciousness Confusion Pupillary abnormalities Altered or absent gag Absent corneal reflex Sudden onset of neurologic deficits Vision or hearing impairment Sensory dysfunction Headache Vertigo Seizures Spasticity .
TRAUMATIC BRAIN INJURY .
8 Severe TBI 9 -12 Moderate TBI 13 -15 Mild TBI .Assessing Injury Severity: GCS Ranges: 3 .
Glasgow Coma Scale Eye-opening ability: Spontaneous (4) To speech (3) To pain (2) No response (1) Motor response: Obeys commands (6) Localizes pain (5) Withdraws (4) Abnormal flexing (3) Abnormal extension (2) No response (1) Verbal response: Oriented (5) Confused (4) Inappropriate words (3) Incomprehensible sounds (2) No response (1) .
CONCUSSION Temporary loss of neurologic function with no apparent structural damage Involves a period of unconsciousness for a few seconds to minutes May be hospitalized for observation .
CONCUSSION OBSERVE FOR headache Dizziness Lethargy Irritability Anxiety Post concussion syndrome .
CONCUSSION Advise to resume normal activities slowly Instruct family to observe the following Difficulty in awakening Difficulty in speaking Confusion Severe headache Vomiting Weakness on one side of the body .
and amount of edema .CONTUSION More severe injury Brain is bruised Unconscious for few secs to mins Symptoms depend on the size.
HEMATOMAS EPIDURAL SUBDURAL INTRACEREBRAL .
EPIDURAL HEMATOMA Lucid interval -.loss of consciousness followed by an interval of apparent recovery Considered an extreme emergency Treatment: Surgery: Burr holes / craniotomy Drain usually inserted .
subacute. or chronic .SUBDURAL HEMATOMA Mainly due to rupture of bridging veins in the subdural space May also be caused by coagulopathy May be acute.
Acute Symptoms develop over 24 to 48 hours Requires immediate intervention Subacute Appear between 48 hours to 2 weeks .
personality changes. Chronic Subdural hematomas From minor injuries Most frequently in the elderly There may be severe headache. alternating focal signs. mental deterioration Treatment: Surgical Evacuation .
INTRACEREBRAL HEMATOMA Bleeding into the substance of the brain Onset may be insidious from neurologic deficit to headache .
Preventing secondary injury .MANAGEMENT OF BRAIN INJURIES All head injured patient is presumed to have a cervical spine injury until proven otherwise.
NURSING DIAGNOSIS AND INTERVENTIONS Ineffective airway clearance Ineffective cerebral tissue perfusion Deficient fluid volume Imbalanced nutrition Risk of injury Impaired skin integrity Disturbed thought process Disturbed sleep pattern Compromised family coping Deficient knowledge .
Potential Complications Decreased cerebral perfusion Cerebral edema and herniation Impaired oxygenation and ventilation Impaired fluid. and nutritional balance Risk of post-traumatic seizures . electrolytes.
usually benign .Brain Tumors Etiology and pathophysiology Either benign or malignant Classified according to tissue of origin Meningioma: occurs outside brain from covering meninges.
glioblastoma. occur from the cranial nerves Gliomas. oligodendroglioma Hemangioblastomas and angiomas. occur from within blood vessels . originate in neural tissue. usually malignant and include astrocytoma.Brain Tumors Acoustic neuroma and optic nerve spongloblastoma.
EEG Symptoms may vary depending on location of tumor . abnormal CT scan. most commonly the lung and breast Clinical findings Subjective: headache that increases when supine or stooping. originate elsewhere in the body.Brain Tumors Metastatic tumors. lethargy Objective: signs of increased intracranial pressure. MRI.
visual hallucinations. motor and sensory focal seizures Occipital region: focal seizures. hemiparesis. blurred vision. focal seizures. tinnitus Parietal lobe: visual loss. papilledema. homonymous hemianopsia . headache. altered thought processes Temporal lobe: seizures. receptive aphasia.Brain Tumors Frontal lobe: personality changes.
Brain Tumors Cerebellar region: loss of coordination. nystagmus Therapeutic interventions Radiation therapy and/or chemotherapy Surgery for partial or complete removal of the lesion Craniotomy with removal of lesion and invaded tissue . tremors.
and neurologic deficits . coping skills.Brain Tumors Stereotactic radiosurgery. and osmotic diuretics to control symptoms Nursing Care of Clients with Brain Tumors ASSESSMENT History from client and family to identify behavioral changes. anticonvulsives. employs computer-directed radiation to eradicate tissue Steroids.
changes in respiratory pattern . decreased pulse rate.Brain Tumors Neurologic status Unilateral nonreactive and/or dilated pupil progressing to bilateral as intracranial pressure increases Signs of increased intracranial pressure Decreased level of consciousness Rapid rise in body temperature.
Brain Tumors Increased systolic pressure.papilledema Vomiting Seizures . widening pulse pressure Restlessness Headache Weakness or paralysis Visual and other sensory disturbances.
related to increased ICP Anxiety related to uncertain prognosis Planning/Implementation Perform routine neurologic assessments .Brain Tumors Analysis/Nursing Diagnoses Ineffective breathing pattern related to compromised neurologic function Decreased adaptive capacity: intracranial.
Provide emotional support for the client and family. refer to additional resources such as clergy and support groups Administer analgesics and antiemetics as ordered Provide small. frequent feedings. supplements. and oral hygiene Provide care for the client requiring brain surgery Obtain consent for surgery and removal of hair After surgery keep the client`s head elevated 30 degrees .
Support respiratory function by encouraging deep breathing, appropriate positioning, and suctioning to maintain the airway Use strict aseptic technique with ICP monitoring Observe dressings for cerebrospinal fluid leakage or hemorrhage Maintain intake and output Use hypothermia as ordered if the client is febrile; fever increases metabolic needs of the brain
Assist client to focus on abilities rather than disabilities Emphasize need for continued health care supervision
Maintains adequate respiratory function Oriented to person, place, and time Establishes effective communication
Management of Patients With Cerebrovascular Disorders
Is a “brain attack”
Needing emergency management, including specific treatments and secondary and tertiary prevention.
Is an emergency
No allowances for worsening are tolerated
Through proven, affordable, acceptable means
In implementable ways across all levels of society
CEREBROVASCULAR DISEASE STROKE DEFINITION
Sudden onset of focal neurological deficit lasting more than 24 hours due to an underlying vascular pathology. Refers to any functional abnormality of the central nervous system that occurs when the normal blood supply to the brain is interrupted.
STROKE 3rd leading cause of death in the U. 2nd leading cause of death in the Philippines .S.
STROKE Two Major Categories Ischemic Vascular occlusion and significant hypoperfusion occur Hemorrhagic Extravasation of blood into the brain .
STROKE Ischemic Large artery thrombosis Lacunar Cardiogenic embolic Cryptogenic Other Hemorrhagic Intracerebral Hemorrhage Subarachnoid Hemorrhage Cerebral Aneurysm Arteriovenous malformation .
Large Artery Thrombosis
The Stroke Continuum
Transient Ischemic Attack
Sudden focal neurologic deficit lasting not more than 24-hours
Stroke in Evolution
Worsening of neurologic signs and symptoms over several minutes. Progressing stroke.
Stabilization of the neurologic signs and symptoms
Stroke Risk Factors
Well-Established Hypertension Transient Ischemic Attack Valvular Heart Disease Atrial Fibrillation Coronary Artery Disease / Myocardial Infarct Carotid Stenosis Diabetes Mellitus Cigarette Smoking Dyslipidemia
Stroke Risk Factors Less Well Established Alcohol Physical Inactivity Lifestyle Factor: Diet .
Clinical Manifestations Visual Field Deficits Motor Deficits Sensory Deficits Verbal Deficits Cognitive Deficits Emotional Deficits .
Approach patient from side of intact field of vision. Instruct/Remind patient to turn head in direction of visual field loss .Visual Field Defects Homonymous Hemianopia Place objects within intact field of vision.
or risky activities in the darkness Place objects in center of patient’s intact visual field Encourage use of cane .Loss of peripheral field of vision Avoid night driving.
Motor Deficits Hemiparesis Place objects within patient’s reach on the non-affected side Instruct patient to exercise and increase strength on non-affected side .
Motor Deficit Hemiplegia Provide ROM exercises Maintain body alignment Exercise unaffected limb to increase immobility .
Ataxia Support patient during initial ambulation Provide supportive device Instruct patient not to walk without assistance .
Dysarthria Provide patient with alternative methods of communicating Allow the patient sufficient time to respond Support patient and family to alleviate frustration .
Dysphagia Test the patient’s pharyngeal reflexes before offering food or fluids Assist the patient with meals Place food on the unaffected side of the mouth Allow ample time to eat .
Sensory Defictis Paresthesias Instruct patient to avoid using this extremity as the dominant limb Provide range of motion to affected areas .
Expressive aphasia Encourage patient to repeat sounds of the alphabet Receptive aphasia Speak slowly and clearly to assist patient in forming the sounds Global aphasia Use simple sentences Use gestures or pictures when able Establish alternative means of communication .
place. and situation frequently Decreased attention span Use verbal and auditory cues to orient patient Impaired ability to concentrate Provide familiar objects .Cognitive Deficits Short and Long term memory loss Reorient patient to time.
Poor abstract reasoning Use non-complicated language Altered Judgement Minimize distracting noises Repeat and reinforce instructions frequently .
Emotional deficits Support patient during uncontrollable outbursts Emotional lability Discuss with patient and family that the outburst are due to disease process Decrease tolerance to stressful situations Encourage patient to participate in group activity .
Anger Provide safe environment Feelings of Isolation Encourage patient to express feelings and frustrations . Depression Provide stimulation for the patient Withdrawal Fear.
Initial Diagnostic Test: Cranial CT scan. Other work-ups: 12 L ECG 2D Echocardiography Electrolytes Carotid Ultrasound Cerebral Angiography Cranial MRI . physical and neurologic examination.Medical Assessment and Diagnostic Findings Complete history.
clopidogrel. dipyridamole Heparin: PTT .5 ASA. ticlopidine.Medical Management Warfarin : INR target 2.
THROMBOLYTIC THERAPY Used to treat ischemic stroke by dissolving the blood clot Recombinant t-PA (rt-PA) must be given within 3 hours of stroke onset. Leads to an overall improvement in functional outcome after 3 months .
Age 18 years or older NIHSS under 22 Within 3 hours or less BP systolic < 185 diastolic < 110 No seizure at onset Not taking warfarin PROTHROMBIN TIME < 15 sec INR < 1.7
Not receiving heparin during the past 48 hours w/o elevated PTT Platelet count > 100,000 CBG 50 to 400 No MI No Intracranial hemorrhage, neoplasm, AV mal, aneurysm
No major surgical procedures within14 days No stroke or head injury within 14 days No gastrointestinal or urinary bleeding within last 21 days
Community Education directed at:
Recognizing symptoms of stroke Obtaining appropriate emergency care Ensure rapid transport to a hospital and initiate therapy within a 3 hour time frame Delays make the patient ineligible for thrombolytic therapy
Rt-PA Dosage and Administration Minimum dose is 0. Maximum dose is 90 mg. Loading dose is infused over 1 minute.9mg/kg. . Remaining dose is administered over 1 hour via an infusion pump. Loading dose is 10% of the calculated dose.
q30 for next 6 hours.Monitoring After Thrombolysis ICU / Acute Stroke Unit Admission VS q15 for 2 hours. then every 16 hours. Side Effect: Bleeding. and 100 mmHg diastolic. BP should be maintained at 180 mmHg systolic. .
Other treatments Reduce ICP with osmotic diuretics Maintaining pCO2 to 30 to 35 mmHg Elevation of the head Intubation if necessary Maintaining cerebral perfusion: MAP Avoiding precipitous drop in blood pressure Neurologic exam to determine if stroke is evolving or complications of treatment develop. .
Endarterectomy for prevention of Ischemic Stroke Carotid Endarterectomy Removal of an atherosclerotic plaque or thrombus from the carotid artery to prevent stroke in patients with occlusive disease of the extracranial cerebral artery Indicated for patients with symptoms of TIA or mild stroke due to SEVERE or 70% to 99% carotid artery stenosis. .
Difficulty in swallowing. Baseline neurologic exam. or other signs of cranial nerve dysfunction .Nursing Management: Carotid Endarterectomy Maintain adequate blood pressure in the immediate postoperative period Monitor Neurologic status. hoarseness.
standing Monitor neurologic status and report changes in mental status Hypertension Postoperative hypotension Hyperperfusion syndrome Intracerebral hemorrahage .COMPLICATIONS OF CAROTID ENDARTERECTOMY Complication Incision Hematoma Nursing intervention Monitor neck discomfor and wound expansion Check blood pressure frequently Monitor BP and signs and symptoms of hypotension Severe unilateral headache improved by sitting.
Nursing Diagnosis: Interventions Impaired physical mobility Shoulder pain Self-care deficits Disturbed sensory perception Impaired swallowing Incontinence Disturbed thought process Impaired verbal communication Impaired skin integrity Interrupted family processes Sexual dysfunction .
Nursing Diagnoses: Interventions Impaired physical mobility Correct positioning Prevent contractures Body alignment Preventing shoulder adduction Changing positions Establishing an exercise program Preparing for ambulation .
transfer devices .Nursing Diagnoses: Interventions Self-Care / Hygiene Eating Devices Non-skid mats to stabilize plates Wide-grip utensils Bathing and Grooming Devices Grab-bars. walkers. wheelchairs. shower and tub seats Toileting Aids Dressing Aids Mobility Aids Canes.
nasal regurgitation. or pooling on one side of the mouth. Thick liquids -----.Nursing Diagnosis: Interventions Managing Dysphagia Must be observed for paroxysms of coughing. food. Sit upright. Smaller boluses of food. chin towards chest .thin liquids. food retained for long periods in the mouth. dribbling.
adequate fluid intake . with impaired sensation in response to bladder filling.Nursing Diagnosis : Interventions Attaining bowel and bladder control Bladder becomes atonic. or control of external urinary sphincter is lost. Intermittent catheterization Constipation / Bowel Control High Fiber diet.
Nursing Diagnosis: Interventions Aphasic Patient Face the patient and establish eye contact Speak in normal manner and tone Use short phrases and pause between phrases Limit conversation to practical and concrete matters Use gestures. pictures. and objects .
.Nursing Diagnosis : Interventions Aphasic Patient Consistent in using same words and gestures Keep extraneous noises and sounds to minimum.
Hemorrhagic Stroke 15% of cerebrovascular disease Two types: Subarachnoid Hemorrhage Aneurysms Intracerebral Hemorrhage AVM Hypertensive Bleeds .
. and cerebral atherosclerosis May also be due to AVM.Pathophysiology: ICH Bleeding into the brain substance or parenchyma Most common in patients with hypertension. brain tumors. and medications.
Common cause of hemorrhage in young people. .Pathophysiology: AVM: Arteriovenous Malformation Abnormality in embryonal development Tangle of arteries and veins in the brain without capillaries – dilation of arteries and veins – rupture.
Pathophysiology: SAH Secondary to intracranial aneurysms Aneurysms – is a dilation of the walls of a cerebral artery that develops as a result of weakness in the arterial wall May be due atherosclerosis May congenital Head trauma – most common cause of SAH .
CLINICAL MANIFESTATIONS Are similar to patients with ischemic stroke. Would depend the site or area of the brain involved .
. Lumbar puncture – can confirm presence of SAH Toxicology drug screen if patient is less than 40 years of age.ASSESSMENT AND DIAGNOSTIC FINDINGS Cranial CT scan – more sensitive than an MRI in detecting blood.
Prevention Managing hypertension Control of other risk factors Smoking Alcohol Intake High cholesterol level .
early decerebrate rigidity V – Deep coma. Mod to severe headache III – Mild focal deficit. Hemiparesis. decerebrate rigidity . confusion IV – Stupor. Slight Nuchal rigidity II – Cranial nerve palsy (III. VI). lethargy. Mild HA. Mod to sev.Hunt-Hess Classification of Subarachnoid Hemorrhages I – Asymptomatic.
treat complications Bed rest with sedation Analgesics Compression stockings . minimize risk of rebleeding Prevent.Medical Management Allow brain to recover Prevent.
Complications Rebleeding Cerebral vasospasm Acute hydrocephalus Seizures .
Cerebral Hypoxia. cerebral blood flow Provide adequate oxygenation Maintain hemoglobin and hematocrit Adequate hydration Avoid extreme hypo/hypertension Controlling seizures . Dec.
Managing Increase ICP Osmotic diuretics Managing complications secondary to osmotic diuretics .
nitroprusside Stool softeners are used . may be given labetalol. nicardipine.Systemic Hypertension Preventing sudden systemic hypertension If elevated.
.Surgical Management ICH: Most frequently via craniotomy SAH: Clipping of aneurysm ASAP Newer endovascular procedures such as Coiling is now available.
or days to several weeks later.Complications: Hydrocephalus Can occur within the first 24 hours. Sudden onset of stupor or coma Managed with ventriculostomy drain to decrease ICP VP shunt for chronic hydrocephalus .
Nursing Diagnosis: Interventions Ineffective cerebral tissue perfusion Monitor closely for neurologic deterioration Pupillary response Motor function Respiration Implementing aneurysm precaustions .
Nursing Diagnosis: Interventions Aneurysm precautions Provide non-stimulating environment Bedrest w/o BRP’s Restrict visitors No strenuous activity including straining Administers all nursing care .
Nursing Diagnosis: Interventions Disturbed sensory perception due to medically imposed restrictions Explanation of the restrictions to reduce anxiety Family requires information and support .
SEIZURE DISORDERS .
sensory. Most seizures are sudden and transient.SEIZURES Are episodes of abnormal motor. autonomic. . or psychic activity (or a combination of these) resulting from excessive discharge from cerebral neurons. Specific causes of seizures are varied and can be idiopathic or acquired. A part or all of the brain may be involved.
hyponatremia. hypoglycemia.pesticides Brain tumor Drug and alcohol withdrawal CVD – leading cause of seizures in the elderly. Acquired Seizures Hypoxemia Fever (childhood) Head injury Hypertension CNS infections Metabolic – renal failure. hypocalcemia Toxic . .
and seizure type.EPILEPSY Group of syndromes characterized by recurring seizures Classified by specific patterns of clinical features. In most cases. including age of onset. Can be primary or secondary – when the cause is known and the seizures is a symptom of an underlying condition. . family history. the cause is unknown or idiopathic.
Clinical Manifestations Depends on the location of the discharging neurons May range from simple starting episode to prolonged convulsive movements with loss of consciousness Partial seizures are focal in origin Generalized are nonspecific in origin Initial pattern of the seizures indicates the region of the brain in which the seizure originates .
International Classification of Epileptic Seizures Generalized Seizures . patient is often confused and hard to arouse and may sleep for hours. loss of bladder/bowel control. rigidity followed by tonic and clonic movements. interruption of respirations. . In post-ictal state.Involve both hemispheres of the brain Tonic-clonic (grand mal) – aura. loss of consciousness.
Absence (petit mal) – brief transient loss of consciousness ( 3-5 secs) with or without minor motor movements of eyes. may result in complete exhaustion and lead to death Febrile seizure – associated with hyperpyrexia. Occurs only once . transient rigidity or jerking of extremities. head or extremities Myoclonic – brief. singly or in groups Status epilepticus – prolonged repetitive seizure without recovery between attacks.
or affective effect Person does not remember the episode when it is over . or Focal Seizures SIMPLE With focal motor. Cognitive. sensory. or autonomic symptoms Without loss of consciousness COMPLEX Begins as simple partial and progress to impairment of consciousness. psychomotor.International Classification of Epileptic Seizures Partial. psychosensory.
Anticonvulsant therapy continued throughout life. diazepam (Valium) given IV to treat status epilepticus Sedatives used to reduce emotional stress .Medical Management PHARMACOLOGIC THERAPY Objective is to achieve seizure control with minimal side effects.
or vascular anomalies. . abscess.Surgical Management Indicated for patients whose epilepsy results from intracranial tumors. Seizures that do not respond to medications.
Video EEG . their frequency and severity.Nursing Process: ASSESSMENT Determining the type of seizures. Developmental history including pregnancy and childbirth Head injury history Imaging: MRI – seizure protocol EEG. factors that precipitate them.
The following are assessed and documented.Nursing Process: Assessment Observe and record the sequence of symptoms. Circumstances Occurrence of aura First thing patient does in a seizure Type of movements Areas of the body involved Size of both pupils Automatisms Incontinence Duration Unconsciousness Paralysis Inability to speak Movements at the end Sleep at the end of the seizure Cognitive status .
Nursing Process: Assessment Ask the following questions: Effect of epilepsy on the patient’s lifestyle Limitations imposed by the seizure disorder Recreational program Social contacts Occupation Coping mechanism .
and raise side rails If an aura precedes the seizure.Nursing Care During a Seizure Provide privacy Ease the patient to the floor Protect the head with a pad to prevent injury Loosen constrictive clothing If in bed. remove pillows. insert oral airway DO NOT attempt to pry open jaws that are clenched in a spasm to insert anything DO NOT attempt to restrain patient during the seizure. Place patient on one side with head flexed forward. Clear secretions .
. Usually a period of confusion after a grand mal seizure. Make sure airway is present.Nursing Care After the Seizure Keep the patient on one side to prevent aspiration. patient should be reoriented to the environment upon awakening. use calm persuasion or gentle restraint. If patient becomes agitated.
Nursing Diagnosis and Interventions DIAGNOSES Risk of injury Fear related to possibility of seizures Ineffective coping mechanisms Deficient knowledge related to epilepsy Complications: STATUS EPILEPTICUS Risk of aspiration related to lowered level of consciousness INTERVENTIONS Preventing Injury Reducing fear of seizures Improving coping mechanisms Providing patient and family education Monitoring and managing complications .
HOME CARE CHECKLIST Take medications as prescribed Keep a medication and seizure chart Have antiseizure medication check regularly Avoid activities that require alertness and coordination Report signs of toxicity Avoid over the counter medications Avoid seizure triggers Take showers instead of tub baths Regular sleep patterns Alcoholic bev. caffeine. fever. hypoglycemia . stress.
possible viral link Most common between ages 20 to 50 years . generally lasts only 2 to 8 weeks but may last longer in older clients Cause unknown.Bell`s Palsy (Facial Paralysis) Etiology and pathophysiology Paralysis that occurs on one side of the face as a result of an inflamed seventh cranial (facial) nerve.
difficulty with articulation. impaired ability to chew and swallow Objective: distortion of face. drooping of mouth on affected side. upward movement of eyeball when closing eye. increased lacrimation .Bell`s Palsy Clinical findings Subjective: facial pain. altered taste. diminished blink reflex.
massage. and electric stimulation to maintain circulation and muscle tone Prevention of corneal irritation with eyedrops and use of protective eye shield .Bell`s Palsy Therapeutic interventions Prednisone therapy Heat.
extent of facial paralysis Nutritional intake and the ability to chew and swallow .Bell`s Palsy Nursing Care of Clients with Bell`s Palsy Assessment Presence or absence of blink reflex and ability to close the eye Facial pain.
manually closing the eye.Bell`s Palsy Analysis/Nursing Diagnoses Pain related to inflammation or compression of facial nerve Risk for injury related to absent or diminished blink reflex Body image disturbance related to change in facial appearance Planning/Implementation Teach prevention of corneal irritation by using artificial tears. and applying an eye shield Teach importance of keeping face warm .
small. and encourage favoring the unaffected side while eating . frequent feedings. institute only when acute phase is over Encourage ventilation of feelings Support nutritional status by providing privacy.Bell`s Palsy Teach gentle massage of face. simple exercises such as blowing.
Bell`s Palsy Evaluation/Outcomes Maintains corneal integrity Expresses a positive body image States pain is reduced .
Trigeminal Neuralgia (TIC Douloureux) Etiology and pathophysiology Incidence higher in women of middle and older age Disorder of the fifth cranial (trigeminal) nerve characterized by intense knifelike pain along the branches of the nerve .
chin. usually in lip.Clinical findings Subjective: burning or knifelike pain lasting 1 to 15 minutes. or teeth. cold drafs Objective: sudden closure of an eye. twitching of mouth and cheek Therapeutic interventions Anticonvulsants to relieve and prevent acute attacks Injection of alcohol into the ganglion to relieve pain for several months or years until nerve regenerates . pain precipitated by brushing hair. eating.
providing permanent relief for most clients .Trigeminal Neuralgia Surgical intervention Severing of the sensory root of the nerve. which will cause loss of all sensation in the area supplied by the nerve Microscopic relocation of arterial loop that may cause vascular compression of trigeminal nerve Percutaneous radio frequency trigeminal gangliolysis: thermal lesion destroys nerve.
Trigeminal Neuralgia Nursing Care of Clients with Trigeminal Neuralgia Assessment Descriptions of pain and factors that precipitates attacks Effect on activities (e. eating. brushing the teeth) because of fear of precipitating an attack . washing the face.. shaving.g.
Trigeminal Neuralgia Analysis/Nursing Diagnoses Fear related to triggering an attack Pain related to irritation of the trigeminal nerve Altered nutrition: less than body requirements related to reluctance to chew Planning/Implementation Teach factors to limit triggering an attack which can result in exhaustion .
Trigeminal Neuralgia Avoid foods that are too cold or too hot Chew foods on unaffected side Use cotton pads to gently wash face and for oral hygiene Keep the room free of drafts. which the client will not be able to feel . avoid jarring Provide teaching to clients who have sensory loss as a result of treatment Inspection of the eye several times a day for foreign bodies.
Trigeminal Neuralgia Warm normal saline irrigation of the affected eye two or three times a day is helpful in preventing a corneal infection Dental checkups every 6 months. because caries will not produce pain Teach about anticonvulsants and the need for continued medical supervision .
Trigeminal Neuralgia Evaluation/Outcomes Reports decreased severity of attacks Consumes nutritionally balanced diet Develops mechanisms to cope with fear .
unknown virus. and chemical or physical trauma .Parkinson`s Disease (Paralysis Agitans) Etiology and pathophysiology Progressive disorder in which there is a destruction of nerve cells in the basal ganglia and substantia nigra of the brain. which results in dopamine deficiency and subsequent generalized degeneration of muscular function Incidence highest in elderly. cerebral vascular disease. suspected causes include neurotransmitter imbalance (dopamine and acetylcholine).
and eating Generalized tremor commonly accompanied by “pill-rolling” movements of the thumb against the fingers. particularly of large joints. muscular pain. diffuse. dressing. Clinical findings Subjective: mild. emotional lability may be present. stiffness and rigidity. nonintention tremors usually reduced by purposeful movements . depression. but intelligence is usually not impaired Objective Increased difficulty in performing usual activities such as writing.
Parkinson`s Disease Various disorders of locomotion (e. difficulty in rising from sitting position. excessive perspiration) . loss of rhythmic arm swing when walking. constipation.. decreased sexual capacity. shuffling propulsive gait.g. difficulty in swallowing saliva Various autonomic symptoms (e.poorly modulated. bent posture. poorly articulated speech Drooling.. incontinence.g. slow. bradykinesia) Masklike facial expression with unblinking eyes Low-pitched. lacrimation.
especially the elderly Therapeutic interventions Medical regimen is palliative rather than curative Pharmacologic intervention (see Antiparkinson Agents in Pharmacology) Physiotherapy to reduce rigidity of muscles and prevent contractures The role of surgical intervention is limited Destruction of thalamus or globus pallidus for intractable tremor and rigidity Transplantation of tissue of adrenal medulla into brain to produce dopamine and transplantation of fetal tissue has been tried . Dementia and confusion in 15% to 20% of individuals.
gait. facial expression.and bradykinesia Nutritional status Elimination status Horizontal and vertical blood pressures to identify postural hypotension .Parkinson`s Disease Nursing Care of Clients with Parkinson`s Disease Assessment History of onset and progression of symptoms Observations of tremors.
Parkinson`s Disease Analysis/Nursing Diagnoses Impaired physical mobility related to neuromuscular degeneration Risk for injury related to postural changes and bradykinesia Self-esteem disturbance related to loss of independence Risk for aspiration related to dysphagia .
encourage diet rich in nutrient-dense foods such as fruits. and legumes to improve and maintain nutritional status and prevent possible drug-induced nutrient deficiencies Suction to maintain an adequate airway (usually advanced stages) . vegetables. whole grains.Parkinson`s Disease Planning/Implementation Provide a safe environment Teach client or family to cut food into small bitesized pieces or alter the consistency to prevent chocking.
keep head and neck as erect as possible.g. use firm mattress without a pillow. periodically lie prone.Parkinson`s Disease Encourage an adequate intake of roughage and fluids to avoid constipation Teach activities to limit postural deformities (e.. think about posture when walking) Teach activities to maintain gait as normal as possible. utilize cane or walker as necessary .
warms baths. Teach and encourage daily physical therapy to limit rigidity and prevent contractures (e.g.. passive and active exercises) Avoid rushing as stress intensifies symptoms Encourage continuation of medications even though results may be minimal Teach client and family about antiparkinson agents Assist in setting achievable goals to improve self-esteem .
Parkinson`s Disease Evaluation/Outcomes Maintains patent airway Participates in daily exercise program Complies with prescribed medical therapy Remains free from injuries .
stress. progressive disease with periods of remission and exacerbation Cause unknown. viral and immunologic causes have been implicated Onset in early adult life (20 to 40 years). and spinal cord Chronic debilitating. and heat tend to increase symptoms . higher occurrence in females Greater incidence in Caucasians and those living in cold climates Fatigue.Multiple Sclerosis (Disseminated Sclerosis) Etiology and pathophysiology Randomly scattered patches of demyelination in brainstem. cerebrum. cerebellum.
scanning (clipped) speech Shuffling gait. altered position sense. spastic paralysis . fatigue Blurred vision. or euphoria) Objective Charcot`s triad: intention tremor. diplopia Altered emotional affect (depression. ataxia Dysphagia Weakness. nystagmus.Multiple Sclerosis Clinical findings Subjective Paresthesia. increased deep tendon reflexes. apathy.
Multiple Sclerosis Impaired bowel and bladder function Impotence Cognitive loss (advanced stage) Pallor of optic discs. blindness Increased immunoglobulin G (IgG) levels in the CSF MRI indicates demyelination .
cyclophosphamide.Multiple Sclerosis Therapeutic interventions Generally palliative Corticosteroids or ACTH Baclofen is used to control spasticity Interferon beta-1b (Betaseron) Physiotherapy and psychotherapy Carbamazepine for paresthesias and trigeminal neuralgia Immunosuppressive drugs (e. azathioprine) ..g.
Multiple Sclerosis Nursing Care of Clients with Multiple Sclerosis Assessment History of onset and progression of motor and sensory loss Factors that intensify symptoms Neurologic status Analysis/Nursing Diagnoses Risk for aspiration related to impaired swallowing Impaired physical mobility related to spasticity and muscle fatigue .
altered sensations.Multiple Sclerosis Risk for injury related to unsteady gait. and impaired vision Constipation related to immobility and neuromuscular impairment Urinary retention related to spasticity Hopelessness related to progression of the disease .
which can increase symptoms Teach use of assistive devices when carrying out activities of daily living Assist family to understand why client should be encouraged to be active .Multiple Sclerosis Planning/Implementation Incorporate frequent rest periods Avoid hot baths.
Multiple Sclerosis Assist client and family to plan and implement a bowel and bladder regimen Explain the disease process to both client and family in understanding terms Do not encourage false hopes during periods of remission Spend time listening to both client and family. encourage ventilation of feelings .
walker.Multiple Sclerosis Refer client and family to the National Multiple Sclerosis Society Encourage counseling and rehabilitation Explain to client and family that mood swings and emotional alterations are part of the disease process Help client maintain self-esteem Teach how to compensate for problems with gait: walk with feet farther apart to broaden base of support. use assistive devices when necessary (tripod cane. use low-heeled shoes. wheelchair) .
change position frequently Teach how to compensate for difficulty in swallowing. use protective clothing in cold weather. chew well.Multiple Sclerosis Teach how to compensate for loss of sensation: use a thermometer to test water temperature. take small bites. avoid constricting stockings. eat foods of more solid consistency . use a straw with liquids.
provide range-of-motion exercises. and legumes to improve and maintain nutritional status and compensate for nutrient interactions of corticosteroid medications Provide skin care to prevent formation of pressure ulcers.Multiple Sclerosis Provide a diet rich in nutrient-dense foods such as fruits. whole grains. splints . vegetables. turn frequently Prevent dysfunctional contractures.
Multiple Sclerosis Evaluation/Outcomes Maintains a patent airway Remains free from injury Establishes exercise/activity and rest/sleep routine that avoids fatigue Maintains bowel and bladder function Copes with changes in physical abilities and life-style changes .
progressive. neuromuscular disorder with remissions and exacerbations.Myasthenia Gravis Etiology and pathophysiology Chronic. there is a disturbance in the transmission of impulses at the myoneural junction resulting in profound weakness Dysfunction thought to be caused by a reduced number of acetylcholine receptors (AChR) and an alteration of the postsynaptic membrane of the muscle end-plate .
Myasthenia Gravis Autoimmune theory: it is believed that complement and antibodies to AChR cause accelerated destruction and blockage of the AChR Highest incidence in young adult females Myasthenic crisis refers to sudden inability to swallow or maintain respirations because of the weakness of the muscles of respiration .
but disappears with rest. becomes progressively worse with use. nasal smile) .Myasthenia Gravis Clinical findings Subjective: Extreme muscle weakness. dyspnea. dysarthria (difficulty speaking). strabismus. dysphagia (difficulty chewing and swallowing). diplopia Objective Physical: ptosis of the eyelid. myasthenic smile (snarling. weak voice (dysphonia).
edrophonium used to distinguish myasthenic crisis from cholinergic crisis (toxic effects of excessive neostigmine) Therapeutic interventions Medications that block the action of cholinesterase at the myoneural junction .Myasthenia Gravis Diagnostic measures: spontaneous relief of symptoms with administration of subcutaneous neostigmine (Prostigmin) or IV administration of edrophonium (Tensilon).
Myasthenia Gravis X-ray therapy or surgical removal of the thymus may cause partial remission Corticosteroids or ACTH Tracheostomy with mechanical ventilation as necessary in myasthenic crisis Plasmapheresis and immunosuppressives to reduce circulating antibody titer .
factors that intensify symptoms Neurologic status (see Neurologic Assessment) Analysis/Nursing Diagnoses Fatigue related to profound muscle weakness Ineffective airway clearance related to inability to cough or swallow .Myasthenia Gravis Nursing Care of Clients with Myasthenia Gravis Assessment History of onset and progression of motor and sensory loss.
and dysarthria. may be caused by worsening of myasthenia (myasthenic crisis) or overdose of anticholinergic drugs (cholinergic crisis) Have an emergency tracheostomy set at bedside Plan activity to avoid fatigue based on the individual`s tolerance .Myasthenia Gravis Planning/Implementation Administer medications on strict time schedule to prevent onset of symptoms Observe for signs of dyspnea. dysphagia.
these drugs potentiate effects of morphine and may cause respiratory depression .Myasthenia Gravis Teach to avoid people with upper respiratory tract infections. because pneumonia may develop as a result of fatigued respiratory muscles Encourage use of a medical alert card Avoid administering morphine to clients receiving cholinesterase inhibitors.
Myasthenia Gravis Provide emotional support and close client contact to allay anxiety Administer tube feedings to avoid aspiration if client has difficulty swallowing Administer artificial tears to keep cornea moist if client has difficulty closing eyes Encourage client and family to participate in planning care Ensure that client understands the signs and symptoms of myasthenic and cholinergic crises .
provide tracheostomy care. or even request assistance Maintain a patent airway.Myasthenia Gravis Refer client and family to Myasthenia Gravis Foundation and local self-help groups In severe instances anticipate all needs. drink. suction as necessary. maintain mechanical ventilation as ordered . because the client is too weak to turn.
Myasthenia Gravis Evaluation/Outcomes Maintains a balance between activity and rest Maintains effective respiratory function Identifies signs and symptoms of crises .
recovery may take up to a year. some experience residual deficits or die of complications . although most recover.Guillain-Barré Syndrome (Polyradiculoneuritis) Etiology and pathophysiology Changes in motor cells of spinal cord and medulla with areas of demyelination Cause unknown. often follows respiratory or gastrointestinal infection After initial and plateau periods. thought to be linked to immunologic status.
diplopia Objective Paralysis begins in lower extremities. hypertension.g.Guillain-Barré Syndrome Clinical findings Subjective:generalized weakness. paresthesia. ascends within the body. diaphoresis) Abnormal CSF and electrophysiologic studies . tachycardia. maximal deficit usually by 4 weeks Respiratory paralysis Autonomic neuropathy (e. muscle pain..
breath sounds. respiratory rate. and arterial blood gases Neurologic status (see Neurologic Assessment) .Guillain-Barré Syndrome Therapeutic interventions Intravenous therapy with IgG Plasmapheresis Support of vital functions Nursing Care of Clients with GuillainBarre Syndrome Assessment Respiratory function including airway.
Guillain-Barré Syndrome History of any recent illness (particularly viral infections) Onset and progression of symptoms Analysis/Nursing Diagnoses Inability to sustain spontaneous ventilation related to muscle weakness Altered role performance related to lengthy recovery period Impaired physical mobility related to impaired neuromuscular function .
and arterial blood gases Maintain airway and keep tracheostomy set at the bedside Monitor functioning of the respirator and suction as necessary Provide emotional support for the client and family because of the severity of adaptations and lengthy convalescent period . breath sounds.Guillain-Barré Syndrome Planning/Implementation Monitor vital signs.
range-of-emotion exercises. antiembolism stockings Refer client and family to Guillain-Barre Foundation for additional information and community resources Maintains effective respiratory function Remains free from complications of immobility Discusses feelings with family and other health-team members Evaluation/Outcomes . coughing and deep breathing. position changes.Guillain-Barré Syndrome Prevent complications of immobility: skin care.
Amyotrophic Lateral Sclerosis (ALS) Etiology and pathophysiology Progressive. degenerative process involving the corticospinal and anterior horn neurons. with subsequent upper and lower motor neuron effects Occurs more frequently in men than women in the fourth and fifth decades Cause unknown. autoimmune diseases and genetic causes are implicated .
Amyotrophic Lateral Sclerosis Death from respiratory complications frequently occurs within 3 to 5 years Clinical findings Subjective: muscular weakness. spasticity. speaking Outbursts of laughter or crying Abnormal electromyography . atrophy Difficulty in breathing. malaise. fatigue Objective Fasciculations (irregular spasmodic twitching of small muscle groups). chewing. swallowing.
possibly preventing injury or death of neurons .Amyotrophic Lateral Sclerosis Therapeutic interventions Physiotherapy to relieve spasticity Supportive respiratory functions Riluzole (Rilutek) to inhibit glutamate accumulation.
depth.Amyotrophic Lateral Sclerosis Nursing Care of clients with Amyotrophic Lateral Sclerosis Assessment History of onset and progression of symptoms Neurologic status Respiratory status including rate. and effort .
employing supportive devices as needed .Amyotrophic Lateral Sclerosis Analysis/Nursing Diagnoses Inability to sustain spontaneous ventilation related to neuromuscular impairment Anticipatory grieving related to progressive nature of illness Impaired physical mobility related to neuromuscular impairment Planning/Implementation Encourage client to remain active as long as possible.
positioning and consistency of diet to prevent aspiration Provide alternate means of communication as speech declines Allow client to discuss feelings about life support while still able to speak Monitor respiratory function. positioning. increased fluids. coughing and deep breathing exercises. chest physiotherapy.Amyotrophic Lateral Sclerosis Encourage range-of-motion exercises Monitor swallowing ability. and suctioning help prevent complications .
Amyotrophic Lateral Sclerosis Support natural defense mechanisms. especially those rich in the immune-stimulating nutrients selenium and vitamins A. C. encourage a diet consisting of nutrientdense foods. and E Teach the avoidance of situations that may contribute to infection Provide emotional support for the client and family Refer client and family to ALS Association .
Amyotrophic Lateral Sclerosis Evaluation/Outcomes Maintains effective respiratory function Discusses feelings with family and other health team members .
Low Back Pain .
Low Back Pain .
Low Back Pain Pain may be a result of acute or repeated stress on the lower back over a period of years Pain occurs because of degeneration and/or acute injury to the tissue of the lower back Caused by sprain or strain of ligaments and muscles Pain may be felt at the site of the injury or referred Overall health of muscles of the lower back determines the degree of risk for injury as .
Low Back Pain Etiology and pathophysiology Low back pain occurs because of repeated injury and progressive degeneration of the spine The two most common causes of low back pain are mechanical strain (irritation or injury to the disc causing degeneration) and herniation of the nucleus pulposus (putting pressure on the nerve roots) .
Low Back Pain .
poor muscle tone of the lower back. and stress Client will report pain caused by a shift of one vertebra on another or pinching and irritation of the nerve root Muscle spasms are a common symptom .Low Back Pain Assessment Risk factors include but are not limited to: degenerative disc disease. poor body mechanics. sedentary lifestyle. obesity. smoking.
Low Back Pain Pain does not appear at the time of injury but is related to the gradual increase of muscle spasms of the paravertebral tissue The straight leg raise test may not be positive with acute injury but pain is present with radiation to the buttock and leg along the path of the sciatic nerve with chronic injury .
Low Back Pain Planning and implementation The goal of treatment is to improve symptoms and slow progression of the degenerative process Include client and family in plan of care Provide emotional support .
and muscle relaxants Epidural corticosteroid injections may be used if conservative treatment is ineffective . NSAIDs.Low Back Pain Medication therapy Medication therapy includes but is not limited to analgesics.
and contraindications with medication use Teach client about the pain rating scale Teach client the importance of adhering to activity restrictions such as bed rest as indicated Teach client the importance of adhering to gradual to activity restrictions such as adherence with exercise plan . side/adverse effects.Low Back Pain Client education Teach client about expected therapeutic effects.
Low Back Pain Teach client the importance of maintaining ideal body weight Inform client that physical therapy will be part of the rehabilitation process to assist in maintaining muscle strength and flexibility as well as improving muscle tone Teach client the use of heat/cold for comfort .
Low Back Pain Teach client about the importance of adhering to the principles of body mechanics to avoid excessive strain on the lower back Encourage client to sleep on a firm mattress Have client demonstrate correct sleeping position using the principles of body mechanics (side lying or supine with knees and hips flexed) Encourage client to avoid or stop smoking Teach client about use of prescribed brace or corset (if needed) to prevent flexion and extension motions of lower back .
Low Back Pain .
THANK YOU! .
Why monitor ICP?
closed box essentially non-compressible components brain, blood, CSF
vascular resistance maintains constant pressure
Volume pressure curve
Concepts of ICP
Closed Box Concept
Volume Pressure Curve
I C 20 P
Causes of Increased ICP Brain trauma. tumor. cerebrovascular disease. infection. intracerebral bleeding CSF hydrocephalus hydrocephalus . edema Cerebral contusion Cerebral edema with slit ventricles Middle cerebral artery stroke Blood vasodilatation.
Normal ICP ~ 0 – 15 Moderate elevation > 20 mmHg Cerebral Perfusion Pressure Cerebral perfusion calculated CPP = MAP (mean arterial pressure) .ICP CPP > 60 .70 mmHg Necessary for carrying oxygen to brain to prevent ischemia .
Herniation (displacement of brain from normal position) .
tumors. Chesnut et al (2000) All patient GCS <8 Who are these patients? Trauma.Who should we monitor? Guidelines for the Management of Severe Head Injury Bullock. edema. aneurysms Sometimes hydrocephalus Infectious diseases .
The END Time for the Test .
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