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NEUROLOGICAL ALTERATIONS NUR 203 Module C Terms β’ Define Terms associated with neurological alterations: β Headachesβ’ Tension, migraines, cluster β Tumors β benign, cancerous β Infections-meningitis, encephalitis β Head injury β contusions, concussions, fractures, intracranial hemorrhage Terms (cont) β’ Transient ischemic attacks β’ Cerebrovascular accidents β Thrombotic β Hemorrhagic β Embolic β’ Spinal Cord dysfunctions β Spinal cord injuries β Herniated disc Terms β’ Spinal Cord dysfunctions β Spinal Shock β’ Paralysis β Quadriplegic (tetraplegia) β Paraplegic β’ Autonomic Dysreflexia β’ Spasticity β’ Neurogenic bladder/bowel Terms β’ Spinal Cord dysfunctions β Respiratory β Sexual β Infection β’ Neuromuscular dysfunction β β β β Multiple Sclerosis Parkinsonβs Guillian-Barre Amyotrophic Lateral Sclerosis Neuromuscular Dysfunctions β’ β’ β’ β’ β’ β’ Myasthenia Gravis Trigeminal Neuralgia Bellβs Palsy Muscular Dystrophy Cerebral Palsy Neural tube defects VASCULAR HEADACHES β’ Tension Headache β β β β β Results from muscle contraction Tight, band-like discomfort that is unrelenting Pain builds slowly in severity Triggered by fatigue and stress Diagnosis confirmed when they occur more than 15 days a month β’ Treatment: β Stress reduction techniques (bio-feedback, psychotherapy and other methods of stress reduction). Also, correction of poor posture. Cluster Headaches (sometimes classified as a form of migraine) β’ Cyclical pattern of periorbital pain lasting form 4 β 8 weeks and usually occurring in the spring or fall β Headache lasts from 15 minutes to hours and may occur several times a day and may awaken from sleep. Unilateral in nature. β’ Pain is described as deep, boring, intense pain of such severity that the patient has trouble staying still. β’ May develop Hornerβs syndrome β Constricted pupils β Unilateral lacrimation β Rhinorrhea β’ Triggered by consumption of alcohol β’ Treated with 100% oxygen via mask β’ Intranasal Lidocaine may be used Migraine Headache β Typically a βtrue vascular headacheβ β Pain results from vasospasm and ischemia of intracranial vessels. β Unilateral pain, but may alternate sides β Throbbing, pulsatile pain β Photophobia, phonophobia, anorexia, nausea, vomiting and focal neurogenic signs may be present β Aura may precede the event βscintillating scotoma (flashing lights), euphoria, fatigue, yawning, and/or craving for sweets β Can be triggered by relief of intense stress, missing meals, or tyramine rich foods β Patient tries to find relief in a quiet, dark environment β Treatment: avoid precipitating factors β Meds: propranolol, amitriptyline, valporate, verapamil, phenelzine and methysergide taken daily β’ If medical treatment is sought at the time of the event: β β β β β Ergotamine Dihydroergotamine Sumatriptan Chlorpromazine Prochlorperazine β’ Patient teaching for migraines: β β β β β Identify triggers Avoid alcohol Avoid tyramine rich foods Avoid low blood sugars Reduce stress INFECTIOUS / INFLAMMATORY DISORDERS MENINGITIS β’ Inflammation of the meninges of the brain and spinal cord β Bacterial β Aseptic (other infective agentsβusually viral) CLINICAL MANIFESTATIONS β’ Classic symptoms: β β β β Nuchal rigidity Brudzinskiβs sign Kernigβs sign Photophobia β’ Other: fever, tachycardia, h/a, prostration, chills, nausea, vomiting β’ May be irritable at first with progression to confusion, stupor, and semiconsciousness β’ Seizures may occur β’ Petechial or hemorrhagic rash may develop β’ CSF is cloudy with bacterial BRUDZINSKIβS SIGN KERNIGβS SIGN DIAGNOSIS β’ Lumbar puncture: β Bacterial: increased protein, decreased glucose, cloudy, increased leukocytes β Viral: increased protein, normal glucose, clear, increased lymphocytes β’ May culture other areas: blood, wounds, sinuses, etc. TREATMENT β’ Isolate until results of CSF analysis are obtained. β Bacterial is very contagious β’ β’ β’ β’ β’ β’ ABX Anticonvulsants Fluid and electrolyte replacement Monitor for increased ICP Provide quiet environment Analgesics may be avoided if they have CNS depressant actionsβwill mask CNS changes ENCEPHALITIS β’ Inflammation of the parenchyma of the brain and spinal cord. Usually caused by a virus. β Arbovirus encephalitis (transmitted by ticks and mosquitoes) β Herpes simplex virus encephalitis may occur as a complication of measles, chickenpox, or mumps. CLINICAL MANIFESTATIONS β’ β’ β’ β’ β’ β’ β’ β’ β’ β’ β’ Fever Headache Seizures Nuchal rigidity Altered LOC Disorientation Agitation Restlessness or lethargy Drowsiness Photophobia N/V BRAIN ABSCESS β’ A collection of either encapsulated or free pus within brain tissue arising from a primary focus elsewhere (ear, mastoid process, sinuses, heart, distal bones, lungs, bacteremia, etc). MANIFESTATIONS β’ β’ β’ β’ β’ β’ Headache Lethargy Drowsiness Confusion Depressed mental status Symptoms of infection β Fever β Chills Traumatic Brain Injuries β’ Over 2 million traumatic brain injuries occur each year with approximately 500,000 injuries severe enough to cause hospitalization. β’ Approximately 50% of all trauma deaths associated with head injury β’ More than 60% of all vehicular trauma deaths are a result of heat injury Traumatic Brain Injury -Mechanism of Injury β’ Penetrating trauma β’ Blunt trauma β Acceleration β Deceleration β Rotational forces Traumatic brain Injury β Patho β’ Primary injury β’ Secondary injury β’ Goals of care include efforts to reduce morbidity & mortality from primary & secondary injuries Traumatic Brain Injury β Patho. β Primary Injury β’ Occurs at moment of impact β’ May be mild or severe β’ Types of primary injuries: β Contusion, laceration, shearing injuries, and hemorrhage Traumatic Brain Injury β Patho. β Secondary Injury β’ The biochemical & cellular response to the initial trauma β Can exacerbate the primary injury & cause loss of brain tissue not originally damaged β’ Ischemia is the primary culprit in secondary brain injury Traumatic Brain Injury - Patho β Secondary Injury (cont.) β’ Hypercapnia is a powerful vasodilator β Results in cerebral vasodilatation & increased cerebral blood volume & ICP β’ Significant hypotension causes inadequate perfusion to neural tissue β *Not typical to be hypotensive with TBI β If hypotensive, need to rule out internal injuries Traumatic Brain Injury - Patho β Secondary Injury (cont.) β’ Cerebral edema β’ Initial hypertension with severe TBI is common β’ Must control HTN to prevent secondary injury caused by increased ICP β’ Effects of increases in intracranial pressure may be varied. BRAIN INJURY β CEREBRAL HEMATOMAS β’ Extravasation of blood produces a spaceoccupying lesion on the brain and leads to increased ICP β’ Epidural & subdural β Extraparenchymal (outside of brain tissue) β’ Produce injury by pressure effect and displacement of intracranial contents. Epidural Hematoma β’ A collection of blood between the inner table of the skull & the outermost layer of the dura β’ Most often associated with: β Skull fractures β Middle meningeal artery laceration Epidural Hematoma β’ Incidence relatively low β’ Can occur as a result of low-impact injuries (falls) or high-impact injuries (MVAs) β’ Occurs from trauma to the skull & meninges rather than from the acceleration-deceleration forces seen in other types of head trauma Epidural Hematoma (cont.) β’ Clinical manifestations: β Brief loss of consciousness followed by period of lucidity β This lucid period is followed by a rapid deterioration in LOC β Dilated, fixed pupil on the same side as the impact area is a hallmark of EDH β May c/o severe, localized H/A & may be sleepy Epidural Hematoma (cont.) β’ Diagnosis: β Based on clinical symptoms & β evidence of a collection of epidural blood identified on CT scan β’ Treatment: β Involves surgical intervention to remove the blood and to cauterize the bleeding vessels Subdural Hematoma β’ The accumulation of blood between the dura and underlying arachnoid membrane. β’ Most often is related to a rupture in the bridging veins between the brain and the dura. β’ Acceleration-deceleration & rotational forces are the major causes. β’ Often associated with cerebral contusions & intracerebral hemorrhage Subdural Hematoma (cont.) β’ Three types: β Acute, β subacute, and β chronic β’ Based on the time frame from injury to clinical symptoms: Subdural Hematoma - ACUTE β’ Hematoma that occurs after a severe blow to the head. β’ Clinical presentation determined by β the severity of injury to the underlying brain at the time of impact & β the rate of blood accumulation in the subdural space. Subdural Hematoma β ACUTE β’ Observe for deterioration in level of consciousness or lateralizing signs, β such as inequality of pupils or motor movements. β’ Deterioration may be rapid β’ Surgical intervention may include β craniectomy, β craniotomy, or β burr hole evacuation Subdural Hematoma -SUBACUTE β’ Develop symptomatically 2 days to 2 weeks after β’ β’ β’ β’ trauma. Expansion of the hematoma occurs at a rate slower than that in acute SDH. Takes longer for symptoms to become obvious. Clinical deterioration with subacute SDH usually is slower than that with acute SDH Surgical intervention, when appropriate, is the same Subdural Hematoma β CHRONIC β’ This term is used when symptoms appear days or months after injury. β’ Most patients usually are elderly or in late middle age. β’ Patients at risk include: β Patients with coordination/balance disturbances, β Elderly, β Those receiving anticoagulation therapy Subdural Hematoma βCHRONIC β’ Clinical manifestations are insidious β’ Patient may report a variety of symptoms: β Lethargy, absent-mindedness, headache, vomiting, stiff neck, and photophobia, and show signs of TIA, seizures, pupillary changes, or hemiparesis β’ Often not seen as initial diagnosis β’ CT scan can confirm diagnosis of SDH Subdural Hematoma β CHRONIC β’ If surgical intervention required, evacuation of the chronic SDH may occur by: β Craniotomy, burr holes, or catheter drainage β’ β’ β’ β’ Outcome variable Return of neurologic status variable Recovery slow Recurrence frequent Subarachnoid Hemorrhage (SAH) β’ Described as bleeding into the subarachnoid space β’ Usually caused by rupture of a cerebral aneurysm or arteriovenous malformation (AVM). β’ Accounts for 6% to 7% of all strokes β Non-traumatic SAH affects more than 30,000 people in US each year β Incidence > in women & increases with age Subarachnoid Hemorrhage (cont.) β’ Overall mortality rate is 25% with most patients dying on first day after injury. β’ Approximately 2 million people in the US are believed to have an unruptured cerebral aneurysm, the congenital anomaly responsible for most cases of SAH. Subarachnoid hemorrhage (cont.) β’ β’ β’ β’ β’ Known risk factors include: **Hypertension, Smoking, Alcohol use, and Stimulant use SAH β Patho β’ Pathophysiology of two most common causes is distinctly different: β Cerebral Aneurysm β Arteriovenous (AV)Malformation SAH β CEREBRAL ANEURYSM β’ As individual with a congenital cerebral aneurysm matures, β BP rises & β more stress placed on vessel wall β’ Saccular or berry-like & most occur at the bifurcation of blood vessels SAH β CEREBRAL ANEURYSM β’ Vessel wall becomes thin & ruptures, β Sending arterial blood at a high pressure into the subarachnoid space. β’ In other situations, the unruptured aneurysm expands and β places pressure on surrounding structures. SAH β ARTERIOVENOUS MALFORMATION β’ Pathologic features related to the size & location of the malformation. β’ One or more cerebral arteries, known as βfeedersβ feed an AVM β’ Feeder arteries enlarge and increase the volume of blood shunted through the malformation. β’ Large, dilated, tortuous draining veins develop SAH βARTERIOVENOUS MALFORMATION β’ The enlarged veins rupture easily β’ Cerebral atrophy is sometimes also present. β It is the result of chronic ischemia because of the shunting of blood through the AVM and away from normal cerebral circulation SAH β ASSESSMENT β’ Characteristically has an abrupt onset of pain, described as the βworst headache of my life.β β’ Brief loss of consciousness, nausea, vomiting, focal neurologic deficits, and a stiff neck may accompany the headache. β’ The SAH may result in coma or death. SAH β ASSESSMENT β’ May have βwarning leaksβ which go undetected. β’ Symptoms of unruptured AVM may be found in the history β Headaches with dizziness or β Syncope or β Fleeting neurologic deficits SAH - DIAGNOSIS β’ Based on: β Clinical presentation, β CT scan, β’ **Noncontrast CT is the cornerstone of definitive SAH diagnosis β Lumbar puncture SAH β DIAGNOSIS (cont.) β’ CT β In 92% of cases, CT can demonstrate a clot in the subarachnoid space, if performed within 24 hours of the onset of the hemorrhage β’ Lumbar puncture if initial CT negative β CSF after SAH bloody in appearance with a RBC > 1000/mm3. SAH β Cerebral Angiography β’ Cerebral angiography necessary once SAH has been documented β To identify exact cause of the SAH β’ If a cerebral aneurysm rupture is the cause, β angiography essential for identifying exact location of aneurysm in prep. for surgery. β’ If AVM rupture the cause, β angiography necessary to identify the feeding arteries & draining veins SAH β Medical Management β’ Is a medical emergency! β’ Preservation of neurologic function is the goal β’ Initial treatment must always support vital functions β’ Early diagnosis is essential β’ Ventriculostomy is performed to control ICP if the patientβs LOC is depressed. SAH β Medical Management β’ Factors attributing to deaths: β’ 19% - related to direct effects of the initial hemorrhage β’ 22% - rebleeding β’ 23% - cerebral vasospasm β’ 23% β non-neurologic medical complications SAH β Re-bleeding β’ The occurrence of a second SAH in an unsecured aneurysm β’ With conservative therapy, 20 β 30% likelihood of re-bleeding in first month, with highest occurrence on first day after initial bleed β’ Mortality with aneurysmal re-bleeding is 48% to 78% SAH β Rebleeding CONS. MEASURES FOR PREV β’ BP control: β Maintain SBP no greater than 150 mm Hg (individualized based on previous values): β Nitroprusside, metoprolol, Hydralazine β *Rebleeding more associated with variations in BP β’ Prophylactic anticonvulsant therapy SAH β Rebleeding β Surgical Aneurysm Clipping β’ Definitive treatment is surgical clipping β’ β’ β’ β’ β’ w/complete obliteration of aneurysm. Timing is key issue Usually within first 48 hours of rupture Eliminates risk of rebleeding Allows more aggressive therapy post-op Allows for flushing out excess blood & clots to reduce risk of vasospasm SAH β Rebleeding β Surgical Aneurysm Clipping β’ Classification of Subarachnoid Hemorrhage β’ Early surgery recommended for patients with Grade I or Grade II SAH & some patients with Grade III β’ Careful consideration of patientβs clinical situation is necessary in determining if candidate for surgery & optimal time SAH - Rebleeding β’ Surgical procedure involves a craniotomy β’ Requires skill of an experienced neurosurgeon β’ Complications SAH β Rebleeding Surgical AVM Excision β’ Decision for surgical excision depends on the location & size of the AVM β’ Surgical excision of large AVMs includes risk of reperfusion bleeding β’ Postop β low BP maintained to prevent further reperfusion bleeding β’ In large AVMs, 2 β 4 stages of surgery may be required over 6 to 12 months SAH β Rebleeding Embolization β’ Used to secure a cerebral aneurysm or AVM that is surgically inaccessible because of size, location, or medical instability of the patient. β’ Several techniques available β All use a percutaneous transfemoral approach in a manner similar to an angiogram SAH β Rebleeding Pharmacologic Therapy β’ In the Past, β antifibrinolytic agents were suggested (aminocaproic acid) β’ TODAY, β Antifibrinolytic agents are NOT recommended for routine use in SAH SAH β CEREBRAL VASOSPASM β’ Presence or absence of cerebral vasospasm significantly affects the outcome of aneurysmal SAH β’ Estimated that 50% of all SAH patients develop vasospasm β 32% resulting in symptomatic vasospasm & β 15% - 20% result in ischemic stroke or death SAH β CEREBRAL VASOSPASM β’ Onset usually 3 β 5 days after initial bleed & can last for 3 to 4 weeks. β’ Treatment: β Induced hypertensive, hypervolemic, hemodilution therapy β Oral nimodipine; and β Transluminal cerebral angioplasty TRANSIENT ISCHEMIC ATTACKS (TIA) β’ Sudden, brief episodes of neurologic dysfunction caused by temporary, focal cerebral ischemia β’ Lasts less than 24 hours, often as little as 5 β 20 minutes β’ Warning sign of impending CVA CLINICAL MANIFESTATIONS β’ Carotid artery occlusion: weakness or numbness in an arm or leg, aphasia, and visual field cuts β’ Vertebrobasilar circulation: vertigo, diplopia, dysphagia, dysarthria, and ataxia DIAGNOSIS β’ β’ β’ β’ β’ Carotid bruit CT Doppler Cerebral angiogram ECG (looking for A fib if site of emboli formation β’ TEE (looking for site of emboli formation) TREATMENT β’ Antihypertensives β’ Antiplatelet drugs β’ Surgery CEREBROVASCULAR ACCIDENT (CVA OR STROKE) β’ Neurological deficits occur as a result of decreased blood flow to a localized area of the brain. β’ Risk factors: β β β β β β Hypertension Diabetes Mellitus CV disease, a-fib Hyperlipidemia Cigarette smoking, alcohol consumption, cocaine use Obesity ISCHEMIC CVA β’ Occurs when blood supply to a part of the brain is interrupted or occluded. Causes: β Spasm: caused by irritation β Thrombosis: platelets adhere to irregular plaque surfaces β Embolism: traveling clot which becomes lodged in a narrow lumen HEMORRHAGIC CVA β’ Occurs in only 10 % of cases, usually women β’ Results from rupture of a cerebral blood vessel that results in bleeding into the brain tissue or the subarachnoid space CLINICAL MANIFESTATIONS β’ β’ β’ β’ β’ β’ β’ H/A Vomiting Seizures AMS Fever ECG changes Manifestations related to area of injury β’ Motor deficits: β β β β β β Hemiplegia Hemiparesis Flaccidity Spasticity Rigidity Dysphagia β’ Elimination disorders β Bowel β bladder β’ Sensory perceptual deficits β Hemianopia β Agnosia β Apraxia β’ Language disorders β Aphasia β Dysarthria β’ Cognitive and behavioral changes β’ Intellectual: memory and judgment changes β’ Right sided CVA β β β β Impulsive Over estimate their abilities Have decreased attention span Left sided weakness β’ Left sided CVA β Slow, cautious, and disorganized β Right sided weakness β’ Spatial perceptual defects: denial of illness or non functioning body parts; erroneous perception of self; agnosia; apraxia DIAGNOSIS β’ β’ β’ β’ β’ CT MRI Doppler ultrasound Cerebral angiogram Lumbar puncture if not contraindicated TREATMENT β’ Acute phase (first 12 β 72 hours): β β β β β β β β If not hemorrhagic: anticoagulant Thrombolytics, if not hemorrhagic Calcium channel blockers Hyperosmolar solutions Diuretics Anticonvulsants Decadron Antipyretics NURSING DIAGNOSIS β’ ALTERED CEREBRAL TISSUE PERFUSION β Monitor respiratory and airway patency β’ Suction only as needed β’ Lateral low Fowlerβs position (ο HOB 30 to ο― cerebral edema, head in neutral position β improves venous drainage) β’ If risk for hemorrhage or IICP, no coughing, deep breathing β’ If no risk of hemorrhage, cough and deep breathe β’ Oxygen as ordered β’ Monitor Neurologic Status β β β β β β LOC Pupilary response Movement, strength of extremities Babinski Decorticate/decerebrate posturing Changes in LOC β’ Monitor CV status β Assess for fluid overload (rales, SOB, dyspnea) β Fluid restriction (if CO is low, increase fluid based on ADH and aldosterone levels) β Prevent thrombosis of lower extremities (ROM, antiembolic hose, pneumatic compression sleeves β’ Monitor Neuro status β Monitor temp (risk for hyperthermia β Monitor for seizures (place on precautions) β’ Impaired mobility: β Prevent contractures β’ Passive/active ROM β’ TQ2H β’ Prone position 15 β 30 minutes several times daily β’ Monitor for thrombophlebitis β’ Self Care deficit β Encourage use of unaffected side β Teach to dress affected side first β’ Sensory perceptual β β β β β β Keep environment clutter free Well lighted environment Bed in low position Wheels locked Side rails up Keep needed objects of the unaffected side β’ Elimination Bladder β Offer bedpan/urinal every 2 hours β Encourage bladder training β Teach Kegel exercises β Use positive reinforcement Bowel β Encourage fluids (2000 cc/day unless CI) β High fiber diet β Stool softeners β Establish bowel evacuation routine β’ Swallowing β β β β β Sit upright when eating and for 30 minutes after Make sure neck is slightly flexed Pureed or soft diet initially Place food/drink on unaffected side When finished eating, assess mouth for absence of food β Maintain suction at bedside β Minimize distractions so they can concentrate PROGNOSIS β’ Assessment β β β β Neurologic Urinary Orthopedic Bowel Acute Spinal Cord Injury β’ Diagnosis begins with: β a detailed history of events surrounding incident, β precise evaluation of sensory & motor function, & β radiographic studies of the spine β’ Majority occurs in males between 16 & 30 Mechanism of injury β’ β’ β’ β’ β’ Hyperflexion Hyperextension Rotation Axial loading Penetrating injuries Mechanism of injury β’ Hyperflexion β Most often seen cervical area at level of C5 to C6. β Sudden deceleration motions β’ Hyperextension β Involve backward & downward motion of the head β Often seen in rear-end collisions or diving accidents Mechanism of Injury β’ Rotation β’ Often occur in conjunction with a flexion or extension injury β’ Axial loading β Vertical compression β Falls & lands on feet β’ Penetrating injuries β Bullet, knife, etc. β Cause permanent damage by anatomical transection SCI β Patho β’ Result of a mechanical force that disrupts neurologic tissue or its vascular supply or both. β’ Injury process includes both primary & secondary injury mechanism SCI β Patho β’ Primary injury β The neurologic damage that occurs at moment of impact β’ Secondary Injury β The complex biochemical processes affecting cellular function β Can occur within minutes of injury and can last for days to weeks SCI β Patho β’ Several events after a spinal cord injury lead to spinal cord ischemia & loss of neurologic function β’ Leads to: β Ischemia, β elevated intracellular calcium β Inflammatory changes β’ Current research focused on inhibiting secondary processes & preserving functional neurons. SCI β’ Functional Injury of the spinal Cord β The degree of disruption of normal spinal cord function β Depends on what specific sensory & motor structures within the cord are damaged β’ Classified as: β Complete or Incomplete SCI β’ Complete Injury β Results in a total loss of sensory & motor function below the level of injury β’ Incomplete Injury β Results in a mixed loss of voluntary motor activity & sensation below the level of the lesion SCI - Complete Injury β’ Quadriplegia β Injury occurs from the C1 to T1 level β Also known as Tetraplegia β’ Paraplegia β Injury occurs in the thoracolumbar region (T2 to L1) β May have full use of arms SCI β Incomplete Injury β’ Brown-Sequard Syndrome β Damage to one side of the cord β Loss of voluntary motor movement on same side as injury, with loss of pain, temperature & sensation on opposite side β’ Central Cord Syndrome β Motor & sensory deficit more pronounced in upper extremities than in lower. SCI β Incomplete Injury β’ Anterior Cord Syndrome β Loss of motor function, as well as loss of sensations of pain & temperature below level of injury β Below injury, position sense & sensations of pressure & vibrations remain intact. β’ Posterior cord Syndrome β Loss of position sense, pressure & vibration below the level of the injury. β Motor function & sensation of pain & temperature remain intact Spinal Shock β’ The complete loss of all normal reflex activity below the level of injury. β’ Manifestations include: β Bradycardia & hypotension β’ Intensity is influenced by level of injury & β’ duration of this shock state can persist for up to 1 month after surgery β’ *Be careful with positioning Assessment for SCI β’ β’ β’ β’ β’ Airway Breathing Circulation Neurologic Diagnostic Procedures AUTONOMIC DYSREFLEXIA β’ A life threatening complication that may occur with SCI. β’ Caused by a massive sympathetic response to a noxious stimuli such as: β Full bladder, line insertions, fecal impaction β’ Results in: β Bradycardia, hypertension, facial flushing, and headache AUTONOMIC DYSREFLEXIA β’ Treatment aimed at alleviating noxious stimuli β’ If symptoms persist, anti-hypertensive agents can be administered to reduce blood pressure β’ Prevention is imperative and can be accomplished through use of a good B & B program AUTONOMIC DYSREFLEXIA β’ Clinical algorithm for treatment of autonomic dysreflexia β β β β β Positioning Constrictive devices Look for cause BP Catheter/Bowel Medical Management β’ Primary treatment is to preserve remaining neurologic function β’ Interventions Divided into: β Pharmacologic β Surgical β nonsurgical Medical Management β’ Pharmacologic Management β’ Methylprednisolone β Bolus followed by continuous infusion for at least 24 hrs & preferably 48 hrs. β’ Prevents post-traumatic spinal cord ischemia β’ Improves energy metabolism β’ Restores extracellular calcium β’ Improves nerve impulse conduction Surgical Management β’ Laminectomy β’ Spinal fusion β’ Rodding Non-surgical Management β’ Cervical Injury β Gardner-Wells and Crutchfield tongs β Halo Vest β’ Thoracolumbar Nursing Management β’ β’ β’ β’ β’ β’ β’ CV Astute assessment of fluid volume Inotropic or vasopressor support Hypotension/hypertension Bradycardia DVT Loss of thermoregulation (poikilothermy) Nursing Management β’ β’ β’ β’ β’ β’ β’ CV Astute assessment of fluid volume Inotropic or vasopressor support Hypotension/hypertension Bradycardia DVT Loss of thermoregulation (poikilothermy) Nursing Management β’ Pulmonary complications are most common cause β’ β’ β’ β’ of mortality Observe rate, rhythm, pattern ABGs Watch for paralysis/weakness of respiratory muscles airway Nursing management β’ Musculosketal β ROM, PT, OT β Splints β’ Integumentary β’ Elimination Rehabilitation & Maximizing Psychosocial Adaptation β’ Provide dedicated emotional support β’ βfour D syndromeβ β Dependency, depression, drug addiction, and, if married, divorce. β’ Further support given by: β Social workers, occupational therapists, psychiatric clinical nurse specialists, pastors, physical therapists, long-term rehab, support groups. Disc Herniation β’ An intervertebral disc is a pad composed of three parts that rests between the centers of two adjacent vertebrae. β’ Discs provide cushions for spinal movement. β’ Strenuous activity or degeneration of the disc or vertebrae can allow the disc to move from its normal location. Disc Herniation β(cont.) β’ Displacement of intervertebral disc material may be referred to as: β β β β Prolapse, herniation, rupture, or extrusion Disc Herniation (cont.) β’ Ruptured intervertebral discs may occur at any level of the spine. β’ Lumbar discs are more likely to rupture than cervical discs because of the: β Force of gravity; β continual movement in this region; and β improper movements of the spine, as with lifting or turning Description β’ Thoracic disc disorders are the least common β’ More than half of patients give a hx of a previous back injury. β’ Heavy physical labor, strenuous exercise, & weak abdominal and back muscles increase risk β’ Repeated stress progressively weakens the disc, resulting in bulging and herniation Clinical Manifestations β’ Lower back pain that radiates down the sciatic nerve into the posterior thigh. β’ Typically begins in the buttocks & extends down the back of the thigh and leg to the ankle. β’ Can also lead to groin pain β’ Muscle spasms & hyperesthesia (numbness & tingling) in areas of distribution of affected nerve roots Clinical Manifestations (cont.) β’ Pain exacerbated by β straining (coughing, sneezing, defecation, bending, lifting, & straight-leg raising) or β prolonged sitting & β’ Is relieved by β side-lying with the knees flexed. Clinical Manifestations (cont.) β’ Any movement of lower extremities that stretches the nerve causes pain & involuntary resistance β’ Straight-leg raising on the affected side is limited β’ Complete extension of the leg is not possible when the thigh is flexed on the abdomen. β’ May have depression of deep tendon reflexes Diagnostic Findings β’ X-Ray Studies β May show spinal degenerative changes β Usually do not show a ruptured disc β’ Magnetic resonance imaging (MRI) β May show extrusion of disc material into the spinal canal and impingement of a spinal nerve root Diagnostic Findings β’ Discography β Injection of a water-soluble imaging material into the nucleus pulposus β Used to determine internal changes in the disc. β’ Electromyography of the peripheral nerves β To localize the site of the ruptured disc Outcome Management β’ Goals include: β Reducing pain & spasms β Improving mobility β Repairing any structural problems in the spine or discs Control Pain & Spasms β’ Pain usually managed with β β β β β Non-steroidal anti-inflammatory drugs (NSAIDS), muscle relaxants, and at times, narcotics Ice may be used for the first 48 hrs After that heat may be used Control Pain & Spasms- Positioning β’ Semi-sitting position (in a recliner chair) β More comfortable, reduces back strain β promotes forward lumbar spine flexion β’ Supine with pillows under the legs β’ Lateral with thin pillow between knees with painful leg flexed β’ AVOID: β prone position β sleeping w/thick pillows under the head Control Pain & Spasms β’ Physical Therapists β may be able to relieve pain & spasm with stretching exercises & ultrasonic heat treatments β’ Spinal manipulation β Use of the hands on the spine to stretch, mobilize, or manipulate the spine β’ Work space or equipment modifications may be necessary β’ Progressive muscle relaxation exercises β’ For severe lumbar disc problems with leg pain β 2 to 4 days of bed rest on a firm mattress Improve Mobility β’ Most clients do not require bed rest β > 4 days of BR can be debilitating & slow recovery β’ Client taught use of proper body mechanics β’ If have to sit, should change positions often β’ Aerobic activities prescribed to help avoid debilitation β’ Walking, stationary bicycling, & back strengthening β Begin within first 2 weeks after injury (perform for 20 to 30 minutes, 2 or 3 times per week) Improve Mobility β’ Work activities individualized β’ Back brace or corset may be prescribed β Usually not recommended once clinical manifestations are relieved β’ Exercise to strengthen the back and abdominal muscles β helps prevent further problems if the exercises are done daily throughout life Surgical Management β’ Surgery indicated in clients with spinal disc problems when β Sciatica is severe & disabling β Manifestations of sciatica persist without improvement or worsen, and β Physiologic evidence of specific nerve root dysfunction β’ Also used to stabilize spinal fractures Surgical Management (cont.) β’ Chemonucleolysis β Chymopapain - a proteolytic enzyme isolated from papaya latex - is used as a meat tenderizer. β Injected into the disc, it digests the protein in the disc & shrinks it. β Contraindicated in people with multiple allergies & in people allergic to papaya. β Immediate & delayed (after 15 days) allergic responses β Use abandoned by most practitioners Percutaneous Disectomy β’ Herniated disc material can be excised with a trocar to remove the center of the disc. β’ The laser also is used to destroy the damaged disc. Microdisectomy β’ The use of microsurgical instruments to remove the herniated fragment of disc. β’ Results in less trauma to the surgical site compared with stand surgery & more tissue integrity is preserved. Decompressive Laminectomy β’ Term laminectomy is confusing & is used loosely. β’ Laminectomy β Describes complete removal of the bone between the spinous process & the facet; β This is seldom necessary. β’ Laminotomy β More correct term for what is usually done β Describes the creation of a hole in the lamina. Decompressive Laminectomy (cont.) β’ Surgical removal of the posterior arch, of a vertebra, exposing the spinal cord. β’ This procedure gives access to the spinal canal for β Removing a spinal cord tumor β Removing portions of the facets β Decompressing bone infringement on the spinal cord Decompressive Laminectomy (cont.) β’ Foraminotomy β Sometimes is performed to enlarge the intervertebral foramen if it is narrowed & osteophytic processes (overgrowth of bone) entrap the nerve root & impinge on neural structures Spinal Fusion/Arthrodesis β’ Spinal fusion β Describes the placement of bone grafts (bone chips) between vertebrae β New bone that grows fuses the two vertebrae & immobilizes them to reduce the pain. β Usually no more than 5 vertebrae are fused β’ Fusing more than five vertebrae causes considerable loss of movement in the spine Spinal Fusion/Arthrodesis (cont.) β’ Bone graft may be obtained from a bone bank or the anterior-superior iliac crest. β’ During healing, the graft gradually grows into the vertebrae & forms a bone union β’ This bone union causes permanent stiffness in the area. Spinal Fusion/Arthrodesis β’ Lumbar Fusion β Stiffness hardly noticed in the lumbar area after a while β’ Cervical Fusion β Stiffness usually noticeable in the cervical area β’ The client cannot be guaranteed that back pain will be relieved permanently or that further surgery will not be required. Spinal Fusion with Instrumentation β’ Metal rods may be used to straighten & fuse the spine in disorders such as scoliosis or multiple vertebral fractures. β’ Other devices also can be used to provide additional support while the bones heal in a fused manner Complications β’ General potential complications after spinal disc surgery at any level include: β β β β Infection and inflammation, injury to nerve roots, dural tears, and hematoma Complications (cont.) β’ Non-union of the surgical area also is a risk β Is associated with smoking β’ Some surgeons assess serum nicotine levels prior to surgery to reduce risk of non-union & β’ validate statements of smoking cessation Prognosis β’ Patients with severe and disabling leg pain: β Lumbar disectomy often relieves manifestations of pain faster than continued medical management β’ Patients w/o leg pain, β little difference in medical vs surgical relief of symptoms β’ Client preference plays a big role in the technique chosen Preoperative Nursing Care β’ Explain post op limitations, positioning, etc. β’ If fusion is to be done: β Encourage clients who smoke to stop. β Clients need to be evaluated for autologeous blood donation. β’ 2 β 3 units should be donated, the last one at least 1 week before the surgery β Inform client of bone graft site & the additional pain associated it. Post Op β’ Assess: β Dressings, drains β Level of pain & response to analgesia β Neurologic function β compare to baseline Post Op β’ BR for post fusion -Risk for DVT β Compression devices β Observe for & report S/S β’ Assess Wound Site: β Bulging or clear drainage β’ May indicate cerebrospinal fluid leakage β Anterior approach β’ Usual care for abdominal surgery is required Positioning β’ After lumbar fusion β Bed is generally kept flat β’ Log-rolling β Usually beginning about 4 hrs after surgery, then q 2 β 4 hrs thereafter β Ensure safety β Common to have spasms & pain w/turning β’ Analgesics & anti-spasmodics PostβOp β Urinary Retention β’ Common after spinal surgery β β because of pain & spasms & β as a side effect of narcotics. β’ Assess for retention β β Cath prn as ordered Post Op β Paralytic Ileus β’ Most common bowel problem after laminectomy & spinal fusion β Due to lack of peristalsis from a sudden loss of parasympathetic function innervating the bowels & β manipulation of the intestines in anterior approaches β’ Assessment findings β N & V, β hard abdomen, β absence of bowel sounds Paralytic Ileus - Intervention β’ NGT to low intermittent suction β’ NPO β’ Assess at least q 4 hrs HERNIATION SYNDROMES β’ **TO PREVENT HERNIATION: β The goal of neurologic evaluation, ICP monitoring, and treatment of increased ICP Herniation Syndromes β’ Herniation results in shifting of tissue β’ Places pressure on cerebral vessels & vital function centers of the brain. β’ If unchecked, herniation rapidly causes death as a result of the cessation of cerebral blood flow & respirations HERNIATION SYNDROMES β (cont.) β’ Supratentorial Herniation β β β β Uncal Central, or Transtentorial Cingulate Transcalvarial β’ Infratentorial Herniation β Upward transtentorial herniation β Downward cerebellar herniation Herniation Syndromes β UNCAL β’ Most often noted herniation syndrome β’ Unilateral, expanding mass, usually of the temporal lobe, increases ICP, causing lateral displacement of the tip of the temporal lobe. β’ Clinical S/S: β Ipsilateral pupil dilation, decreased LOC, respiratory pattern changes/arrest, contralateral hemiplegia (decorticate/decerebrate) Herniation Syndromes CENTRAL β’ Often preceded by uncal and cingulate herniation β’ Expanding mass lesion of the midline, frontal, parietal, or occipital lobes β’ S/S β Similar to Uncal in late stages Herniation Syndromes β CINGULATE β’ Occurs often β’ Not in itself life-threatening, but if the expanding mass lesion is not controlled, uncal or central herniation will follow. Herniation Syndromes β Transcalvarial β’ The extrusion of cerebral tissue through the cranium β’ In the presence of severe cerebral edema, transcalvarial herniation occurs through an opening from a skull fx or craniotomy site Herniation Syndromes β Upward Transtentorial Herniation β’ Deterioration progresses rapidly β’ Compression of 3rd cranial nerve & diencephalon occurs β’ Blockage of central aqueduct β’ Distortion of 3rd ventricle obstruct CSF flow Herniation Syndromes β Downward Cerebellar Herniation β’ Compression & displacement of the medulla oblongata occur β’ Rapidly results in respiratory & cardiac arrest CHRONIC DISORDERS AMYOTROPHIC LATERAL SCLEROSIS (ALS) β’ Also known as Lou Gehrigβs Disease β’ A progressive degenerative neurologic disease characterized by weakness and wasting of the involved muscles, without any accompanying sensory or cognitive changes. β’ Unknown cause β’ Affects men more than women, usually between the ages of 40 β 60. CLINICAL MANIFESTATIONS β’ Musculoskeletal: β β β β β β β weakness and fatigue βheavinessβ of the legs fasciculations (focal muscle twitching) Uncoordinated movements Loss of motor control in the hands Spasticity Paresis β Hyperreflexia β Atrophy β Problems with articulation β’ Respiratory β Dyspnea β Difficulty clearing the airway β’ Nutrition β Difficulty chewing β Dysphagia β’ Emotion β Loss of control, liability β’ Cognitive β Intellect is not affected β Remains alert and mentally intact throughout the course of the disease β’ Death is usually resultant from pneumonia β’ Diagnosis is made with an EMG TREATMENT β’ Supportive β’ Riluzole (Rilutek): drug which extends the life by a few months β’ Respiratory compromise usually results within 2 β 5 years of diagnosis INTERVENTIONS β’ Mobility β β β β β β ROM Stretching exercises Splints Ankle boots Wheelchair Frequent rest periods to decrease fatigue β’ Nutrition β β β β β β β β Suction at bedside Rest before meals Upright to eat and 30 minutes after Semisolid food Frequent meals Soft cervical collar to keep head upright Enteral feedings Syringe with short, small bore tubing (placed on anterior aspect of tongue, used for giving liquids) β’ Breathing β β β β β β β Mechanical ventilation as necessary Elevate HOB TQ2H Oxygen Breathing exercises Incentive spirometry Suctioning as needed β’ Communication β Speech therapy β Hand held computers β Pointer held with teeth and use of a picture board β Word charts β Eye blinks MULTIPLE SCLEROSIS β’ β’ β’ β’ β’ β’ Chronic, progressive disorder of the CNS. Weakness Remission Progression Glial scar tissue (hard, sclerotic plaque) Loss of function CLINICAL MANIFESTATIONS β’ musculoskeletal β β β β β β β β Fatigue (most common and often most disabling) Limb weakness ( loss of muscle strength) Ataxia Intention tremors Spasticity Muscular atrophy Dragging of the foot Foot drop β’ Urinary β β β β β Hesitancy Frequency Retention Recurrent UTIβs Incontinence β’ Gastrointestinal β β β β β Difficulty chewing Dysphagia Diminished or absent sphincter control Bowel incontinence Constipation β’ Respiratory β Diminished cough reflex β Respiratory infections β’ Sensory β β β β β β β β β β β Blurred vision Optic neuritis Diplopia Nystagmus Eye pain Visual field defects Vertigo/ loss of balance and coordination Nausea Numbness Parasthesias (numbness or tingling) Diminished sense of temperature/ desensitized touch sensation β’ Neurologic β β β β β β Emotional lability/ mood changes/ depression Forgetfulness Apathy Irritability Impaired judgment Dysarthria (speech problems) β’ Diagnosis β β β β History CSF evaluation MRI Optic/Auditory testing (shows slowed nerve conduction) TREATMENT β’ β’ β’ β’ β’ Corticosteroids Interferon Plasmapheresis Surgery Diet therapy INTERVENTIONS β’ Respiratory β CDB Q 2 β 4 H β Elevate HOB 90o to eat β’ Immobility β PT for walking and hydrotherapy β’ Gastrointestinal β Stool softeners β Encourage activity β Maintain fluid intake β’ Skin β β β β Assess every shift TQ2H Keep linen clean and dry Massage around bony prominences β’ Vision β Assess acuity β SR elevated, bed in low position, wheels locked β Eye patch with diplopia β’ Urinary β β β β Administer appropriate meds Intermittent catheterization Assess for infection Increase fluids to 3000 cc/day if allowed β’ Teaching β Factors which cause exacerbation β’ Hyperthermia β’ Stress β’ Infection β’ pregnancy MUSCULAR DYSTROPHY β’ A group of genetic disorders involving gradual degeneration of muscle fibers β’ Progressive weakness and skeletal muscle wasting, accompanied by disability and deformity β’ Types: 1. Pseudohypertrophic MD (Duchene MD) 2. Facioscapulohumeral MD (LandouzyDejerine) CLINICAL MANIFESTATIONS β’ Evidence of muscle weakness usually appears at 3-4 yrs β’ May have history of delayed motor development, especially walking β’ First symptom may be : difficulties in running, riding a bike β’ Develop characteristic rising from squatting or sitting position on floor (Gowerβs sign) TREATMENT β’ Supportive measures β β β β Physical therapy Orthopedic procedures Use of braces for spine and lower extremities Breathing exercises MYASTHENIA GRAVIS β’ A chronic, progressive autoimmune disease characterized by fatigue and severe muscle weakness of the skeletal muscles, that worsens with exercise and improves with rest β’ Manifestations result from a loss of Ach receptors in the postsynaptic neurons of the neuromuscular junction CLINICAL MANIFESTATIONS β’ Primary feature: increasing weakness with β’ β’ β’ β’ β’ sustained muscle contraction Ptosis (drooping of upper eyelid) Diplopia (double vision) Facial weakness (snarls when smiling) Dysphagia dysarthria β’ Weakness and fatigue β’ Decreased function of hands, arms, legs, β’ β’ β’ β’ β’ β’ and neck muscles Weakening of intercostals Decreased diaphragmatic movement Breathlessness and dyspnea Poor gas exchange Inability to chew and swallow Decreased ability to move tongue DIAGNOSIS β’ Based on clinical presentation and response to anticholinesterase drugs β’ TENSILON TEST TREATMENT β’ Anticholinesterase drugs β Pyridostigmine (mestinon) β Neostigmine (Prostigmine) β’ Immunosuppressive therapy (corticosteroids) β’ Plasmaphoresis β’ Thymectomy COMPLICATIONS β’ Myasthenic crisis: caused by undermedication β β β β β Sudden marked rise in B/P due to hypoxia Increased heart rate Severe respiratory distress and cyanosis Absent cough and swallow reflex Increased secretions, increased diaphoresis, increased lacrimation β Restlessness, dysarthria β Bowel and bladder incontinence β’ Cholinergic Crisis: caused by excessive medication β Weakness with difficulty swallowing, chewing, speaking and breathing β Apprehension β N/V/D/abdominal cramps β Increased secretions and saliva β Sweating, lacrimation, fasciculations, and blurred vision NURSING CARE β’ β’ β’ β’ Airway management Suction at bedside ABGs Endotracheal intubation if ventilatory support is needed β’ Administer edrophonium chloride (Tensilon) to determine type of crisis β’ Monitor electrolytes, I&O, daily weight β’ Tube feeding if unable to eat CEREBRAL PALSY β’ Impaired muscular control due to abnormality in the brain resulting in abnormal muscle tone and coordination. Physical signs: β β β β β β Poor head control after 3 months Stiff or rigid arms or legs Pushing away or arching back Floppy or limp body posture Cannot sit up without support by 8 months Use of only one side of body, or only the arms to crawl β Clenched fists after 3 months BEHAVIORAL SIGNS β’ Extreme irritability or crying β’ Failure to smile by 3 months β’ Feeding difficulties β Persistent gagging or choking when fed β After 6 months of age, persistent tongue thrusting CLINICAL MANIFESTATIONS β’ Delayed gross motor movement (universal β’ β’ β’ β’ β’ manifestation) Abnormal motor performance Altered muscle tone Abnormal posture Abnormal reflexes Associated disabilities and problems INTERVENTIONS β’ β’ β’ β’ β’ β’ Mobilizing devices Surgery Speech therapy Dental care Hearing aids Physical therapy PARKINSONβS DISEASE β’ Progressive, degenerative disease characterized by disability from tremor and rigidity β Depletion of dopamine CARDINAL FEATURES β’ β’ β’ β’ β’ β’ Tremor at rest Rigidity Bradykinesia (slow movement) Flexed posture of neck, trunk, and limbs Loss of postural reflexes Freezing movement OTHER CLINICAL MANIFESTATIONS β’ β’ β’ β’ β’ β’ β’ Skin problems Heat intolerance Postural hypotension Constipation Dementia Anxiety Depression TREATMENT β’ Dopaminergics β Levodopa β Carbidopa-levodopa (Sinemet) β’ Anticholinergics β Trihexphenidyl (Artane) β Benztropine (Cogentin) β’ Dopamine Agonists β Bromocriptine (Parlodel β Pergolide (Permax) β’ Surgery: β Pallidotomy β Sterotaxic thalamotomy β Autologous adrenal medullary transplant (doesnβt work well) β Fetal tissue transplant (better results) INTERVENTIONS β’ Mobility β β β β β ROM PT (individualized) Ambulate qid Assistive devices Provide for safety β’ Communication β β β β Allow time to speak Encourage deep breathing before speaking Speech therapy Alternative methods of communication β’ Sleep β β β β Quiet environment Position of comfort ROM to decrease rigidity Stay awake during day (meds may interrupt normal sleep cycle) β’ Nutrition β β β β β β β β Calorie count/weekly weight Assess swallowing ability Soft, solid food appropriate for the individual Massage facial and neck muscles before eating Sit upright for feeding and 30 minutes after Suction at bedside Adequate roughage/fiber Small, frequent meals β’ Elimination β β β β Drink 3000 cc/day if possible Increased fiber Increase mobility to stimulate peristalsis Stool softeners/suppositories β’ Self care: β Encourage independence but set time limits β Keep items in reach β Give a time frame to allow the patient to do their own care Bellβs Palsy βPatho & Etiology β’ Affects motor aspects of the facial nerve, (7th β’ β’ β’ β’ cranial nerve). Most common type of peripheral facial paralysis. Affects women & men in all age groups Most common between ages 20 & 40 yrs. Results in a unilateral paralysis of the facial muscles of expression. Bellβs Palsy βPatho & etiology β’ No evidence of a pathologic cause. β’ Facial paralysis central or peripheral in origin. β’ Central facial palsy is an upper motor neuron paralysis or paresis. β Client cannot voluntarily show teeth on paralyzed side but can show them with emotional stimulation. β’ Called voluntary emotional dissociation Bellβs Palsy β Clinical Manifestations β’ Typical findings on affected side include: β Upward movement of the eyeball on closing the eye (Bellβs phenomenon) β Drooping of the mouth β Flattening of the nasolabial fold β Widening of the palpebral fissure β Slight lag in closing the eye β’ Eating may be difficult Bellβs Palsy β Outcome Management β’ No known cure. β’ Palliative measures include: β Analgesics if discomfort occurs from herpetic lesions β Corticosteroids to decrease nerve tissue edema β Physiotherapy, moist heat, gentle massage, & stimulation of the facial nerve β Corneal protection w/artificial tears, sunglasses, eye patch Neurological Clinical Assessment β’ History β’ Physical examination components β β β β β Level of consciousness (LOC) Motor function Pupillary function & eye movement Respiratory patterns Vital signs Bellβs Palsy β Recovery/Prognosis β’ Clients experiencing Bellβs Palsy often think they have had a stroke. β Reassure client β’ Prognosis β Most clients recover within a few weeks w/o residual manifestations. β’ If permanent facial paralysis occurs, surgery may be necessary. β Anastomosis of the peripheral end of the facial nerve with the spinal accessory or hypoglossal nerve may allow closure of the eye & restore tone to face Trigeminal Neuralgia β’ Chronic irritation of the fifth cranial nerve β’ Trigeminal nerve has 3 division & neuralgia may occur in any one or more of these divisions β Opthalmic, β maxillary, & β mandibular Trigeminal Neuralgia β Etiology β’ Causes can be intrinsic or extrinsic lesions within the nerve itself β Ex: multiple sclerosis β’ Extrinsic lesions are outside the trigeminal root & include mechanical compression by β Tumors, vascular anomalies, dental abscesses, or jaw malformation Trigeminal Neuralgia β Clinical Manifestations β’ Characterized by intermittent episodes of intense β’ β’ β’ β’ pain of sudden onset. Pain is rarely relieved by analgesics Tactile stimulation, such as touch & facial hygiene, & talking may trigger an attack More prevalent in the maxillary and mandibular distributions & on the right side of the face. Bilateral trigeminal neuralgia is rare Trigeminal Neuralgia βDiagnosis β’ None of the current diagnostic studies identify trigeminal neuralgia β’ CT scan, MRI, & angiography can identify a causative lesion. β’ Diagnosis made on basis of in-depth history, w/attention paid to triggering stimuli & nature & site of the pain. Trigeminal Neuralgia β Nursing Considerations β’ Careful history is obtained regarding triggering stimuli β’ Dental hygiene & nutritional intake are evaluated Trigeminal NeuralgiaβOutcome Mgt β’ Anticonvulsant agents often prescribed as initial treatment β Carbamazepine (Tegretol) β phenytoin β’ These drugs may dampen the reactivity of the neurons within the trigeminal nerve β’ For some clients, these medications are all the treatment that is needed β’ Monitor liver enzymes before & during therapy β’ Use caution if hx of alcohol abuse Trigeminal NeuralgiaβOutcome Mgt β’ Baclofen (Lioresal) β An antispasmodic that may be used alone or in conjunction with anticonvulsants. β’ Narcotics are not particularly effective β’ Help client use & improve any pain control strategy they have developed. β’ Provide emotional support Trigeminal NeuralgiaβOutcome Mgt β’ Surgery includes β Nerve blocks with alcohol & glycerol β Peripheral neurectomy & β Percutaneous radio-frequency wave forms β’ Relief obtained not always permanent β’ 0ften better tolerated by elderly or debilitated clients β Therefore, present later with symptoms Trigeminal Neuralgia β Outcome Mgt β’ More invasive techniques involve major surgical procedures (craniotomy): β’ Microvascular decompression β Removing the vessel from the posterior trigeminal root β’ Rhizotomy β Actual resection of the root of the nerve TN β Outcome Mgt β Surgical Complications β’ Same as with any surgical procedure β’ Facial weakness & paresthesias β’ If facial anesthesia present after surgery β β β β Test food before placing in mouth Assess for aspiration & advance diet slowly Water jet device instead of toothbrush Visit dentist soon β’ If corneal reflex impaired β Eye care Guillian-Barreβ Syndrome (GBS) β’ Once thought to be single entity characterized by inflammatory peripheral neuropathy β’ Now understood to be a combination of clinical features with varying forms of presentation & multiple pathologic processes. GBS (cont.) β’ Most cases do not require admission to CCU β’ Prototype of GBS, known as acute inflammatory demyelinating polyradiculoneuropathy (AIDP) involves rapidly progressive, ascending peripheral nerve dysfunction leading to paralysis & maybe respiratory failure GBS (AIDP) β’ Because of the need for ventilatory support, AIDP is β’ β’ β’ β’ one of the few peripheral neurologic diseases that necessitate a critical care environment. Annual incidence of GBS is 1.6 β 1.9 per 100,000 persons. Occurs more often in males Most commonly acquired demyelinating neuropathy. Clusters of cases reported following 1977 swine flu vaccinations GBS - Etiology β’ Precise cause unknown β’ Syndrome involves an immune-mediated response β’ Most patients report a viral infection 1 to 3 weeks before the onset of clinical manifestations, usually involving upper respiratory tract. GBS - Etiology β’ Numerous triggering events include: β β β β β β Viral infections Bacterial infections Vaccines Lymphoma Surgery Trauma GBS - Pathology β’ Affects: β motor & sensory pathways of the peripheral nervous system, β as well as the autonomic nervous system functions of the cranial nerves. β’ Believed to be an autoimmune response to antibodies formed in response to a recent physiologic event. β’ Once temporary inflammatory reaction stops, myelinproducing cells begin the process of re-insulating demyelinated portions of PNS. β’ Degree of axonal damage is responsible for the degree of neurologic dysfunction. GBS β Assessment & DX β’ Symptoms include: β Motor weakness β Paresthesias & other sensory changes β Cranial nerve dysfunction β’ (especially oculomotor, facial, glossopharyngeal, vagal, spinal accessory, and hypoglossal); and β Some autonomic dysfunction GBS β Assessment & DX β’ Abrupt onset of lower extremity weakness that progresses to flaccidity and ascends over a period of hours to days. β’ Motor loss usually symmetric, bilateral, and ascending β’ In the most severe cases, complete flaccidity of all peripheral nerves, including spinal and cranial nerves, occurs. GBS β Assessment & DX β’ Admitted to hospital when lower extremity weakness prevents mobility β’ Admitted to CCU when progression of weakness threatens respiratory muscles. β’ DX based on clinical findings plus CSF analysis & nerve conduction studies. β’ Diagnostic finding is elevated CSF protein with normal cell count GBS β Assessment & DX β’ Frequent assessment of respiratory system β’ Most common cause of death is from RESPIRATORY ARREST β’ As disease progresses & respiratory effort weakens, intubation & MV are necessary β’ Continued, frequent assessment of neurologic deterioration is required until the patient reaches the peak of the disease & plateau occurs. GBS β Medical Mgt β’ No curative treatment available β’ Disease must run its course, which is characterized by ascending paralysis that advances over 1 to 3 weeks & then remains at a plateau for 2 to 4 weeks. β’ Plateau stage followed by descending paralysis & return to normal or near-normal function. GBS β Medical Mgt β’ Main focus is the support of bodily functions & prevention of complications β’ Plasmapheresis often used in attempt to limit severity & duration β Contraindicated if hemodynamically unstable β’ IV imunoglobulin may be used β’ Steroids may be used GBS β Nursing Mgt (cont.) β’ Support all normal body functions until the patient can do so on his or her own β’ Requires extensive long-term care, β recovery can be a long process GBS β Nursing Mgt (cont.) β’ Focuses on: β β β β Maintaining surveillance for complications Initiating rehabilitation Facilitating nutritional support, Providing comfort & emotional support GBS βMonitor for Complications β’ Once intubated and on MV β Observe for pulmonary complications β’ (ie: atelectasis, pneumonia, pneumothorax β’ Autonomic dysfunction, dysautonomia β Can produce variations in HR & BP β Hypertension and tachycardia may require beta-blocker therapy GBS β Initiating Rehabilitation β’ Immobility may last for months β’ Usual course of GBS involves: β average of 10 days of symptom progression β 10 days of maximal level of dysfunction β Followed by 2 to 48 weeks of recovery β’ Patient requires physical & occupational rehabilitation because of the problems of long-term immobility. GBS β Rehab (cont.) β’ Facilitating Nutritional Support β Usually accomplished through use of enteral feeding β’ Patient education β’ Participation in a neurologic rehabilitation program (if necessary) GBS β Providing Comfort & Emotional Support β’ Pain control β A safe, effective, long-term solution to pain management must be identified. β’ Extensive psychologic support β’ *GBS does not affect the LOC or cerebral function β Patient interaction & communication are essential elements of the nursing management plan. Clinical Manifestations Using the Glasgow Coma Scale Coma, Persistent Vegetative State Other Complications Glasgow Coma Scale (GCS) β A tool for assessment β’ For LOC only β’ Not a complete neurological exam β’ Evaluation of 3 categories β Eye opening β Verbal response β Motor response Rapid Neurologic Examination β’ Organized, thorough, & simple. β’ Performed accurately & easily at each assessment point β’ Conscious Patient β’ Unconscious Patient Rapid Neurologic Assessment β Conscious Patient β’ β’ β’ β’ β’ β’ β’ β’ Exam should take less than 4 minutes LOC Facial Movements Pupillary function & eye movements Motor assessment Sensory VS Change in status Rapid Neurologic Assessment β Unconscious Patient β’ Assessment takes 3 to 4 minutes β’ Initial efforts are directed at achieving maximal β’ β’ β’ β’ β’ arousal of the patient LOC Pupillary assessment Motor examination Respiratory pattern VS Neurologic changes Associated with Intracranial Hypertension β’ Increasing ICP can be identified by changes in: β’ LOC (*1st Sign of deterioration in a conscious patient) β Increased restlessness, confusion, agitation, decreased responsiveness β’ β’ β’ β’ Pupillary Reaction Motor Response Vital Signs Respiratory Patterns Diagnostic Procedures β’ β’ β’ β’ β’ β’ β’ Computerized tomograpy (CT Scan) Magnetic resonance imaging (MRI) Cerebral Angiography Myelography Cerebral Blood Flow Studies Electrophysiology Studies Lumbar Puncture COMA β’ A state of unconsciousness in which both wakefulness and awareness are lacking β’ A symptom, rather than a disease β Occurs as a result of some underlying process β’ Can be produced by a wide variety of both neurologic & non-neurologic conditions β’ Comprises a continuum of many levels COMA - Etiology β’ Structural neurologic lesions β’ Metabolic and toxic conditions β’ Psychiatric disorders COMA β Structural Lesions β’ Vascular lesions β Ischemic & hemorrhagic strokes β’ Trauma β Loss of consciousness may occur immediately or may develop several daysβweeks after injury β’ Brain tumors and brain abscesses β Compression of neurologic structures β Often accompanied by motor paralysis COMA β Metabolic & Toxic Conditions β’ Accounts for more than half of all cases of coma COMA β Cardiopulmonary Decompensation Any cardiopulmonary condition can precipitate a state of coma by threatening the state of oxygenation of cerebral tissue COMA β Poisoning & Alcohol β’ May occur as the result of self-administration, accidental ingestion, industrial exposure, or homicidal administration β’ Drug overdose β 30% of cases in ED β’ Symptoms depend on substance ingested β’ Alcohol may not be cause of coma in inebriated patient β Trauma, cerebral hemorrhage, subdural hematoma β’ Thiamine deficiency COMA β Hypertensive Encephalopathy/HTN Crisis β’ Sudden onset, usually following hx of kidney disease, severe HTN, or both COMA - Meningitis β’ Common cause of coma β’ Fever or signs of meningeal irritation β’ Abrupt onset, severe HA followed by loss of consciousness β’ Hx of infectious process affecting middle ear or paranasal sinuses should raise suspicion of meningitis. CLINICAL MANIFESTATIONS β’ Classic symptoms: β β β β Nuchal rigidity Brudzinskiβs sign Kernigβs sign Photophobia β’ Other: fever, tachycardia, h/a, chills, nausea, vomiting, seizures β’ May be irritable at first with progression to confusion, stupor, and semiconsciousness COMA β’ β’ β’ β’ β’ β’ β’ Encephalitis Post-convulsion Other Metabolic Disturbances Hyper/hypoglycemia Hepatic coma Pneumonia Ecclampsia, various endocrine disorders; hyperthermia, & electrolyte, acid-base, or water imbalance. COMA β Patho. β’ β’ β’ β’ Slight or moderate cortical depression Complete cortical suppression Midbrain depression Brain stem depression COMA βAssessment & DX β’ Detailed serial neurologic examinations β’ CT or MRI β Usually readily identify structural causes β’ Lumbar Puncture (unless contraindicated by signs of increased ICP) β Analysis of CSF pressure & content β **CT precedes Lumbar Puncture to identify patients at risk for brain herniation β’ Laboratory studies to identify metabolic or endocrine abnormalities Medical Management β’ Identification & tx of underlying cause β’ Emergency measures to support vital functions & prevent further neurologic deterioration β’ Protection of airway & ventilatory assist β’ If cause not known β Thiamine (at least 100 mg), glucose, & a narcotic antagonist suggested Medical Mgt (cont.) β’ Prognosis depends on β cause of the coma & β length of time unconsciousness persists. β’ Best prognosis is associated with early arousal β’ Metabolic coma - better prognosis than coma caused by a structural lesion β’ Traumatic coma - better outcome than non-traumatic COMA β’ Clinical Manifestations of Metabolically & Structurally Induced Coma COMA β Nursing Mgt β’ **Patient is totally dependent on the health care team β’ Interventions directed toward: β Assessment β’ changes in neurologic status & β’ clues to the origin of the coma β Supporting all body functions β Maintain surveillance for complications β Providing comforting and emotional support β Initiating rehabilitation measures COMA β Eye Care β’ Blink reflex is often diminished or absent β Results in drying & ulceration of the cornea β’ Interventions to protect the eyes β Instill saline or methyl cellulose lubricating drops & taping eyelids shut β Instilling saline drops q 2 hr & applying a polyethylene film over the eyes Coma Stimulation Therapy β’ Based on the belief that structured brain stimulation fosters brain recovery PERSISTENT VEGETATIVE STATE (PVS) β’ State of unconsciousness in which wakefulness is β’ β’ β’ β’ present but awareness is lacking Absence of any ascertainable cerebral cortical function Complete or partial hypothalmic & brain stem autonomic functions are present, Sleep-wake cycles are present There is complete unawareness of self & the surrounding environment Diagnostic Criteria for PVS β’ No evidence of awareness of self or environment β’ Inability to interact with others β’ No evidence of sustained, reproducible, purposeful, or voluntary behavioral response to visual, auditory, tactile, or noxious stimuli β’ No evidence of language comprehension or expression Diagnostic Criteria for PVS(cont.) β’ Intermittent wakefulness manifested by presence of sleep-wake cycles β’ Sufficiently preserved hypothalmic & brain stem autonomic functions to permit survival with medical & nursing management β’ Bowel & bladder incontinence β’ Variably preserved cranial nerve reflexes and spinal reflexes PVS - Assessment & DX β’ Differentiating feature between PVS & coma is the wakefulness of the PVS patient β’ Most difficult differential diagnosis is between PVS & a locked-in state β Locked-in state patient is conscious but unable to communicate because of severe paralysis Differentiating characteristics of PVS & other related conditions PVS - Assessment & DX β’ Diagnosis must be made by a specialist with expertise in this area. β’ Moral, ethical & legal issues pertaining to PVS are the subject of much debate β’ Positron-emission tomography (PET) & electroencephalography (EEG) are used to support diagnosis PVS - Medical Mgt β’ No treatment to reverse PVS is known β’ Coma sensory stimulation is being studied β’ Prognosis depends on the cause of the underlying brain disease β’ For patient in a PVS that resulted from degenerative or metabolic brain disease β No chance for recovery is possible β’ Average life expectancy is 2 to 5 years PVS - Medical Mgt β’ Collaboration between physicians & family to determine appropriate level of medical management β’ Decisions must be made regarding: β β β β Resuscitation status Medications (including antibiotics & O2) Hydration, nutrition, and Long-term placement PVS - Nursing Management β’ Primarily comprised of: β β β β Performing a detailed neurologic assessment Providing supportive & hygienic measures, and Preventing complications of immobility Psychosocial & informational support of the family REYE SYNDROME (RS) β’ A disorder defined as toxic encephalopathy associated with other characteristic organ involvement. β’ Very uncommon now- review from PEDS ASSESSMENT OF INTRACRANIAL PRESSURE INTRACRANIAL PRESSURE β’ Intracranial space comprises 3 components: β brain substance (80%), β cerebrospinal fluid (CSF) (10%), β and blood (10%). β’ Under normal conditions, the ICP is maintained below 15 mm Hg mean pressure INTRACRANIAL PRESSURE β’ Monroe-Kellie hypothesis proposes that β an increase in volume of one intracranial component must be compensated by a decrease in one or more of the other components so that total volume remains fixed ICP β’ As ICP rises, small increases in volume may cause major elevations in ICP. β’ Cerebral blood flow (CBF) corresponds to the metabolic demands of the brain & is normally 50 ml/100 g of brain tissue/minute. β’ Brain requires 15% to 20% of the resting cardiac output & 15% of the bodyβs O2 demands ICP β’ MAP of 50 β 150 does not alter CBF when autoregulation is present β’ Acidosis (causes cerebrovascular dilation) β Hypoxia, hypercapnia, ishcmia β’ Alkalosis (causes cerebrovascular constr.) β hypocapnia β’ Changes in metabolic rate β Increases increase CBF β Decreases decrease CBF Operative Terms Burr hole Craniotomy Craniectomy Cranioplasty Supratentorial Intratentorialy Mgt of Intracranial Hypertension β’ Once identified, therapy must be prompt β’ Most current evidence suggests that ICP generally must be treated when it exceeds 20 mmHg β’ All therapies are directed toward reducing the volume of one or more of the components (blood, brain, CSF) that lie within the intracranial vault. ICP β’ Major goal of therapy is to determine the cause of the elevated pressure, and if possible, to remove the cause β’ In absence of a surgically treatable mass lesion, intracranial hypertension is treated medically. ICP β Nsg Interventions for intracr. HTN β’ β’ β’ β’ Patient positioning Maintaining normothermia Controlled ventilation to ensure normal PaCO2 Administering meds β Keep CPP near 80 mmHg to provide adequate blood supply to the brain β CPP = MAP β ICP β’ Performing ventricular drainage ICP β Nursing Interventions POSITIONING β’ Head elevation increases venous return β May place some patients at risk for intracranial HTN & cerebral ischemia caused by increases of CPP β’ Recent trend is to individualize head position to maximize CPP & minimize ICP measurements ICP β Nursing Interventions POSITIONING β’ Obstruction of jugular veins or an increase in intrathoracic or intrabdominal pressure is seen as increased pressure through the open venous system, β impeding drainage from the brain and increasing ICP. ICP β Nursing Interventions POSITIONING β’ Positions that decrease venous return from the head must be avoided if possible. β’ Examples of positions to avoid: β β β β Trendelenburg, prone, extreme flexion of the hips, angulation of the neck ICP β Nursing Interventions POSITIONING β’ If have to place in Trendelburg β Monitor ICP & VS closely β’ May use mechanisms to reduce intracranial pressure β Sedation and/or ventricular drainage ICP β Nsg Interventions β’ Associated with increased ICP: β β β β β Use of PEEP > 20 cm H20 pressure Coughing, suctioning Tight tracheostomy tube ties Valsalva maneuver Care activities performed one after another β’ Associated with decreased ICP: β Family contact & gentle touch ICP β BP control β’ Maintenance of arterial BP in the high normal range is essential in the brain-injured patient. β’ Inadequate perfusion pressure decreases the supply of nutrients & O2 requirements for cerebral metabolic needs. β’ A blood pressure too high increases cerebral blood volume and may increase ICP ICP β BP Control MEDICATIONS β’ Sedatives β small, frequent doses β’ Antihypertensive agents β Avoid use of nitroprusside & NTG (potent peripheral & cerebral vasodilators) β’ To reduce vasodilating effect of anti-hypertensives, co-treatment with beta-blockers β Metoprolol, Labetalol SEIZURES β’ Episodes of excessive and abnormal discharges of electrical activity within the CNS β’ Epilepsy is a syndrome of recurrent, paroxysmal episodes of seizure activity β Partial β Generalized PARTIAL (FOCAL, LOCAL) SEIZURES β’ Simple partial seizures β Seizure activity occurs in a specific body part β’ Jacksonian March β Sensory phenomena β Autonomic manifestations β Psychic manifestations GENERALIZED SEIZURES β’ Absence: sudden, brief sensation of motor activity accompanied by a blank stare and unconsciousness β’ Myoclonic:sudden, uncontrollable jerking movements of either a single muscle group or multiple groups, sometimes causing the patient to fall. Patient loses consciousness for a moment and is then confused postictally TONIC CLONIC SEIZURE β’ β’ β’ β’ May or may not have an aura Sudden loss of consciousness Tonic phase Clonic phase β’ Tonic-clonic phase β’ Clonic seizures: rhythmic muscular contraction and relaxation lasting several minutes β’ Tonic seizures: an abrupt increase in muscular tone and muscular contraction β’ Tonic-Clonic βGrand Malβ STATUS EPILEPTICUS β’ Continuous seizing activity and may have brief periods of calm. Because the patient is in a constant state of seizing, they may develop hypoxia, acidosis, hypoglycemia, hyperthermia, and exhaustion β’ Complex Partial Seizures β With automatisms: purposeless repetitive activities β Complex partial evolving to secondary generalized PHARMACOLOGY β’ Phenytoin (Dilantin) β Therapeutic level: 10 β 20 mcg β SE: nystagmus, diplopia, ataxia, slurred speech, insomnia, dizziness, gingival hyperplasia, n/v/c, measles like rash, rust colored urine, Steven Johnsonβs syndrome β’ Phenobarbital β Therapeutic range: 10 β 40 mcg/ml β SE: drowsiness, dizziness, h/a, n/v/d, jaundice, mild rash β Nursing Interventions β’ No abrupt withdrawal β’ Use caution β’ No alcohol, CNS depressants, other barbiturates β’ Medic alert identification β’ No calcium products β’ Deep IM β’ Nursing interventions for Dilantin: β β β β Donβt give IM Incompatible with dextrose Not faster than 50 mg/min IV Monitor for hypotension, bradycardia, bradypnea β Do not give po with milk, calcium, antacids, MOM β Hold tube feeding β Teaching Neural Tube Defects Neurological Dysfunctions HYDROCEPHALUS β’ Blockage of the drainage of cerebrospinal fluid from the ventricles of the brain or from impaired absorption of CSF within the subarachnoid space β’ Many causes CLINICAL MANIFESTATIONS β’ Bulging fontanels with or without head β’ β’ β’ β’ β’ β’ enlargement Dilated scalp veins Frontal protrusion (Bodding) Eyes rotated downward (setting sun sign) Sluggish pupils, unequal response to light Irritability Poor feeding β’ β’ β’ β’ Lower extremity spasticity Difficulty swallowing, feeding Shrill, high pitched cry seizures TREATMENT β’ Preferred procedure: ventriculoperitoneal shunt β’ Preoperative β Elevate HOB β Prevent crying which increases intracranial pressure β Avoid jarring, bouncing or any activity that will increase intracranial pressure β Head measured daily β Monitor fontanels for bulging β’ Ventriculoperitoneal shunt β’ Post op care β Position flat, on unoperative side β Monitor for increased ICP (indicates obstruction of shunt) β NPO restriction for 24 β 48 hours β IV fluid caution to prevent overload β’ Revised as child grows β’ Complications β Infection β Malfunction due to obstruction SPINA BIFIDA OCCULTA β’ A neural tube defect that is not visible externally β’ Skin depression or dimple, port wine angiomatous nevi, or dark tufts of hair may be the only visible sign β’ No treatment is necessary unless neurologic problems develop (abnormal weight gain, problems with bowel or bladder, etc.) SPINA BIFIDA CYSTICA β’ Neural tube defect with external sac-like protrusion β Meningocele: encases meninges and spinal fluid but no neural elements β Myelomeningocele: contains meninges, spinal fluid and nerves MYELOMENINGOCELE β’ Located anywhere on the neural tube β’ May be covered with a fine membrane, the dura, meninges, or skin β’ Most frequently occurs in the lumbar or lumbar sacral area β’ 80-85 % have associated hydrocephalus PATHOPHYSIOLOGY β’ Failure of the neural tube to close during the first 28 days of pregnancy β’ Can also occur due to splitting of the already closed tube due to increase in cerebrospinal fluid pressure during the first trimester CLINICAL MANIFESTATIONS β’ Usually not uniform on both sides β’ Affects bowel and bladder sphincters (constant dribbling or overflow incontinence; lack of bowel control or rectal prolapse β no rectal temps for these children) β’ May have lower joint deformities (from contractures in utero) DIAGNOSIS β’ β’ β’ β’ MRI CT Ultrasound Elevated maternal alpha fetoprotein level (done at 16 β 18 weeks gestation) PREOPERATIVE CARE β’ Warm incubator without clothing (clothing may irritate β’ β’ β’ β’ β’ β’ β’ sac) Moist dressing changes every two hours (0.9% Normal Saline) Cleanse carefully if soiled Keep prone Diapering is contraindicated until repaired ROM (restricted to foot, ankle and knee) Prone position when held by parents (may not be able to do) Tactile stimulation (caressing, stroking, other comfort measures) POSTOPERATIVE CARE β’ β’ β’ β’ Maintain prone or side lying position Frequent vital signs and daily weights Measure head circumference daily Examine fontanels for signs of tension or bulging β’ Catheterization for urinary retention β’ Monitor for infection PROGNOSIS β’ Assessment β β β β Neurologic Urinary Orthopedic Bowel Complications β’ β’ β’ β’ β’ β’ Increased intracranial pressure Unconsciousness Systemic Infections Neurogenic Shock Seizure disorders Others INCREASED ICP β’ Risk factors: head injury, brain tumors, cerebral bleeding, hydrocephalus, and edema from surgery or injury β’ Most often associated with a space occupying lesion PATHOPHYSIOLOGY β’ The skull is a hard, bony vault filled with brain tissue, blood, and CSF. A balance b/w these 3 maintains the pressure w/in the cranium β’ B/C the bony skull canβt expand, when one of the 3 components expands, the other 2 must compensate by decreasing in volume in order for the total brain volume to remain constant INCREASED INTRACRANIAL PRESSURE β’ Decreased LOC is the first sign β β β β β Alert Lethargic Obtunded Stuporous Semicomatose DECORTICATE POSTURING DECEREBRATE POSTURING MORE CLINICAL MANIFESTATIONS β’ Pupillary responses: β Early: diplopia, blurring, decreased acuity β’ Changes in motor function: β Early: progressive muscle weakness β Late: decorticate, decerebrate, flaccid β’ Headache β Early: vague but present β Late: accompanied by projectile vomiting without nausea β’ B/P and Pulse: β Early: relatively stable β Late: increased SBP while DBP stays the same (widened pulse pressure); bradycardia β’ Temperature: β Early: normal, then increases β hyperthermia followed by hypothermia as CSF increases β’ Respirations: β Early: normal β Late: decreased at first together with increased SBP and decreased pulse. As ICP increases, the character changes: deeply yawning, signing, Cheyenne Stokes. DOLLβS EYES β’ β’ β’ β’ Unconscious patientβs only Hold eyes open Briskly turn head side to side If eyes move in the opposite direction than the way the head is turned, then the patient has positive dollβs eyes. This is normal β’ If they stay fixed at midline, this is negative. β’ Do not perform on a patient with a cervical fracture TREATMENTS β’ β’ β’ β’ β’ β’ β’ β’ Mannitol Corticosteroids Antipyretics Barbiturates to induce coma Anticonvulsants Antibiotics IV fluids (NS is best but ½ NS may be used) Surgery SEIZURES β’ Episodes of excessive and abnormal discharges of electrical activity within the CNS β’ Epilepsy is a syndrome of recurrent, paroxysmal episodes of seizure activity β Partial β Generalized PARTIAL (FOCAL, LOCAL) SEIZURES β’ Simple partial seizures β Seizure activity occurs in a specific body part β’ Jacksonian March β Sensory phenomena β Autonomic manifestations β Psychic manifestations β’ Complex Partial Seizures β With automatisms: purposeless repetitive activities β Complex partial evolving to secondary generalized STATUS EPILEPTICUS β’ Continuous seizing activity and may have brief periods of calm. Because the patient is in a constant state of seizing, they may develop hypoxia, acidosis, hypoglycemia, hyperthermia, and exhaustion ACTIONS DURING SEIZURES β’ Airway β β β β β Loosen clothing around neck Turn to side if possible Do not force anything into the mouth Oxygen as ordered via mask Suction as needed β’ Injury β β β β Bed in low position with wheels locked Side rails up Padded side rails If standing, lie down; place padding under headβ protect the head from injury β Remove potentially harmful objects β Teaching β’ Donβt smoke alone or in bed, avoid alcohol, avoid being tired, grab the bars in the bathroom, donβt lock doors, avoid excessive caffeine
