NURS 265 Exam 3

• -decreased LOC(lethargy to coma) -restlessness, irritability, confusion -headache -projectile N&V -change in speech pattern/slurred speech -dilated nonreactive pupils or constructed nonreactive pupils -ataxia -seizure -abnormal posturing -Cushing's triad: severe HTN, widened pulse pressure, bradycardia • Key sx of increased ICP • Symptoms of increased ICP -severe HTN, widened pulse pressure, bradycardia • What is Cushing's triad • Most at risk during 1st 72 hours after stroke onset • Risk for increased ICP after stroke • -elevate HOB and keep head in midline neutral position -oxygen -avoid sudden and acute hip or neck flexion -space out care -prevent unnecessary coughing or suctioning -quiet environment for headache -keep lights low for photophobia -closely monitor VS and glucose • Interventions for increased ICP • 10-15 mm hg • Normal ICP levels • 20 • A sustained ICP or greater than _______ mm hg is considered detrimental and neurons start to die • Brainstorm herniation into foramen of monro • If brain edema from increased ICP remains untreated, this happens • Hydrocephalus • Increased CSF in brain caused by obstruction of the normal CSF pathway from edema, an expanding lesion such as a hematoma, or blood in the subarachnoid space, leading to increased ICP • Primary- occurs at time of injury and results from the force within the tissue caused by a blunt or penetrating force Secondary- any processes that occur after initial injury and worsen or negatively influence pt outcome • Primary vs secondary brain damage • Focal- confined to specific area of brain and causes localized damage, detected by CT or MRI Diffuse-characterized by damage throughout many areas of brain, not initially detected by CT bc this type is microscopic damage, MRI may detect • Primary brain injury can be a focal or diffuse injury. • Hypotension and hypoxia, intracranial HTN, and cerebral edema • Most common causes of secondary brain injury • epidural hematoma • a collection of blood in the space between the skull and dura mater resulting from arterial bleed • subdural hematoma Can be acute, subacute, or chronic • collection of blood under the dura and above arachnoid mater resulting from venous bleed, bleed is slower than an epidural hematoma • Presents within 48 hr after impact • Acute subdural hematoma • Occurs between 48 hr and 2 weeks after impact • Subacute subdural hematoma • Occurs after 2 weeks to several months after impact. Has highest mortality rate bc it goes unnoticed. • Chronic subdural hematoma • Intracerebral hemorrhage • The accumulation of blood within brain tissue caused by tearing of small arteries and veins in the subcritical white matter • Mild Traumatic Brain Injury (MTBI) • What level of brain injury is Characterized by blow to the head, transient confusion or feeling dazed and disoriented, and one or more of these conditions: loss of consciousness for up to 30 min, loss of memory for events immediately before of after accident, and/or focal neurological deficits that may or may not be transient, no evidence of brain damage on CT • moderate traumatic brain injury • What level of brain injury is Characterized by a period of loss of consciousness for 30 min to 6 hr and a GCS of 9-12. Often(not always) focal or diffuse injury seen on CT. Post trauma amnesia may last up to 24 hours • Severe traumatic brain injury • What level of brain injury is characterized by a GCS score of 3-8, and a loss of consciousness longer than 6 hr. Focal and diffuse damage to brain, brain vessels, and brain ventricles are common • 9-12 • GCS score for moderate traumatic brain injury • 3-8 • GCS score for severe traumatic brain injury • Appears dazed or stunned. Loss of consciousness 30 min. Headache. N&V. Gait problems. Visual problems. Dizzy. Photophobia. Sensitive to noise. Fatigue. Mentally foggy and slowed down. Difficulty concentrating and remembering. Drowsy. Either sleeping more or less than usual. Emotional changes such as irritability, sadness, nervousness, depression, or more emotional. Sx can last days weeks or months(post-concussion syndrome) but usually resolve within 72 hours • Sx of mild traumatic brain injury • ABCs. Because TBI is occasionally associated with cervical spinal cord injuries, all patients should be treated as if they have fun until proven otherwise. Indicators of spinal injury: head tilt, sensory perception and mobility loss, tenderness along spine, Cheyne stokes. Monitor capnography. High CO2 can cause cerebral vasodilation and ICP. Low CO2 can cause vasoconstriction and ischemia. Document any dysrhythmias, hypotension, or hypertension. Temp may occur. Therapeutic hypothermia may be started regardless of presence of fever. • Assessing a TBI pt • brain stem dysfunction at level of pons • Pinpoint and non responsive pupils are indicative of • occipital lobe • Loss of vision is damage to • papilledema • swelling and increased blood flow of the optic disc; always a sign of increased ICP • Left side • Injury to right brain causes sx of • Therapeutic hypothermia • therapy started after Trumatic brain injury where we rapidly cool the patient to a core temperature of 89.6 and 93.2 for 1-2 days after primary injury. This reduces brain metabolism and prevents secondary brain injury. • Record vital signs every 1 to 2 hours or more often. IV fluids. Document and report presence of cardiac dysrhythmias, hypertension, and hypotension. Watch for hyperthermia. Watch ABGs. Lidocaine IV for cough suppressant so ICP isn't increased. • Interventions for preventing and detecting secondary brain injury related to TBI • Positioning of TBI pt • organ donation c enter. • If pt has severe TBI, contact • Coma of known cause is established by history, clinical examination, lab testing, and neural imaging. 2. Normal or near normal body temperature. 3. Normal systolic blood pressure. 4. At least one neurologic examination. • 4 things needed to diagnose brain death • Mannitol and lasix boluses. Opioids May be used to reduce agitation with ventilator pt. Use fentanyl • Drug therapy for TBI and increased ICP • For mannitol Use through filtered tubing or draw up in filtered syringe to eliminate microscopic crystals. Monitor intake and output w/ foley and kidney function. Serum electrolytes and osmolarity drawn every 6 hr. • Mannitol and lasix considerations • Sensory perception loss. Only play DVDs for 15 min at time. They get lost • If a large lesion of the parietal lobe is present, patient may experience what • Severe headache, persistent or severe nausea and vomiting, blurred vision, drainage from the ear or nose, increased weakness, slurred speech, progressive sleepiness, worsening headache, unequal pupil size • If mild TBI has these sx, take back to ER • Pituitary Dysfunction. SIADH or DI. • Complication of brain tumor • No • Are benign tumors cancerous ? • Benign, malignant, or metastic. Supratentorial or infratentorial • How are brain tumors classified. • Difference between Supratentorial or infratentorial Tumor • meningioma • Most common benign tumors. Arise from coverings of brain (the meninges) and caused displacement of brain tissue. • Can remove but they tend to come back. • Meningioma surgery • Pituitary tumor • Benign Tumor that occurs in anterior lobe that account for one fourth of brain tumors and may cause endocrine dysfunction, more often in middle aged adults • Adenoma • Most common type of pituitary tumor • visual disturbances and pituitary signs such as SIADH or DI, loss of body hair, infertility, and headaches • Sx of pituitary tumor • acoustic neuroma aka cerebellar pontine angle (CPA) tumors • benign tumor on the auditory nerve (8th cranial nerve) that causes vertigo, tinnitus, and hearing loss, women more likely to get • Hearing loss, facial pain and weakness, dysphagia, decreased gag reflex, ataxia and dysarthria, bradycardia, hypotension, nystagmus, hoarseness, apnea • Brain stem tumor sx • HEADACHE, seizure, vomiting unrelated to food intake, changes in visual acuity or field, diplopia, hemiparesis, hypokinesia, aphasia, changes in personality or behavior • Cerebral tumor sx • Supratentorial: paralysis, seizures, memory loss, cognition impairment, vision changes infratentorial: ataxia, autonomic NS dysfunctions, vomiting, drooling, hearing loss, vision changes • Neurological sx differences between Supratentorial and infratentorial tumors • Chemo therapy. Phenytoin, dexamethazone, PPI to prevent stress ulcers • Drug therapy for brain tumors • stereotactic radiosurgery • Technique in which a single large dose of radiation is delivered under precise 3D guidance to destroy vascular abnormalities and small brain tumors. • NDAIDS, tobacco, alcohol or anticoagulants for 5 days before surgery. NPO for 8 hr before surgery. • Before craniotomy, check that pt hasn't had any • Monitor for ICP. assess neuro status and VS q 15-30 min for 4 hours then every hour. Periorbital edema and bruising may occur and treated with cold compresses. Irrigate effected eye with warm saline to provide comfort. Cardiac dysthymia monitoring. Keep HOB up 30 degrees with pt with Supratentorial craniotomy to promote venous drainage. For infratentorial craniotomy, keep patient flat or up 10 degrees. Assist with side lying turning every 2 hours to reduce strain on neck area incision. May have drain placed for couple days. Normal drain output is 50 ml/ hr • Post op care of craniotomy • Otitis media, acute or chronic sinusitis, tooth abscess, immunocompromised pt receiving cancer tx is also at risk • Infections liked to meningitis • Meningitis • inflammation of the meninges of the brain and spinal cord, can lead to permanent nerve damage or ICP • Viral • What type of meningitis is the most common type • viral meningitis(aseptic meningitis) , HIV, mumps, varicella • meningitis caused by a virus and not as severe as pyrogenic meningitis, what can cause ? • Cryptococcus neoformans Meningitis. Use IV antifungals • Most common fungal infection that affects the CNS of patients with aids, fungal sinusitis can also be a cause • Streptococcus pneumoniae and neisseria mengingitidis • Most frequently involved organisms responsible for bacteria meningococcal meningitis • Meningicoccal Meningitis(bacterial) • A meningitis medical emergency with a high mortality rate often within 24 hours and unlike other types is highly contagious • Areas of high population density such as college dorms, military, and other crowded living area, 16-21 years at risk. Get vaccine at 12 years old. • Where are bacterial meningitis outbreak's more likely to happen • nuchal rigidity • stiffness in cervical neck area • nuchal rigidity, photophobia, phonophobia, headache, myalgia(muscle aches), N&V, possible altered LOC w confusion. • Sx of meningitis • Positive Kernigs and Brudzinski sign and classic nuchal rigidity CSF analysis(give broad-spectrum antibiotic before lumbar puncture) • How to diagnose meningitis • Enterovirus • Maculopapular rash is associated with which meningitis • Neisseria menin gitidis • Petechiae rash is associated with which meningitis • Kernig's sign • a diagnostic sign for meningitis marked by the person's inability to extend the leg completely when the thigh is flexed upon the abdomen and the person is sitting or lying down • Brudzinski's sign • pain with resistance and involuntary flex of hip/knee when neck is flexed to chest when lying supine • SIADH, seizure, SIRS, shock, increased ICP, vascular dysfunction • Complications of meningitis • SIRS (systemic inflammatory response syndrome) • Complication of meningitis when A reaction to either endotoxin produced by infecting bacteria or activation of immune cells by infecting organisms causes a drop and BP and tachycardia • Low BP, tachycardia, coagulopathy May result such as DIC. Thrombi may Block circulation in the small vessels of hands and feet, leading to gangrene. • SIRS sx • Sx of meningitis • Vaccine for HIB , mumps, pneumococcal, meningococcal, varicella. Thorough hand washing. • How to prevent meningitis • ABC. Monitor & document neuro status, vascular status, and VS q 2-4 hr for increased ICP. Seizure precautions. Manage pain. Vascular assessment. Record intake and output and monitor weight to ID any fluid retention. Position carefully and perform ROM q4h. Decrease environmental stimuli. Maintain bed rest with HOB up 30. Transition based precautions if bacterial Droplet precautions for bacterial. • Meningitis interventions • Started on broad spectrum ATB until culture back. 2 week IV ATB course. Mannitol. Anti epilepsy drugs. Possible steroids. • TX of meningitis • People who have been in close contact with N. Meningitidis should have prophylactic tx of rifampin, Cipro, ceftriaxone. Preventative tx of rifampin for H. Influenzae • Concerns for family members of pt with meningitis • Droplet. Stay at least 3 feet away if no mask on. Pt transported outside the room should wear a mask. • Precautions for bacterial meningitis • encephalitis • inflammation of the brain usually caused by a virus that usually effects the cerebrum, brain stem, and cerebellum. Can be life threatening and lead to neuro disabilities such as learning disability, epilepsy, memory or fine motor deficits. • ICP and herniation • Death can occur in encephalitis from • Arboviruses • Viral infection that can cause encephalitis and is transmitted through mosquito bite or tick • Herpes simplex 1. Most pt have history of cold sores. • Most common and more fatal viral encephalitis cause • Fresh water areas or in soil • Amoebic encephalitis can be found • High fever. N&V Stiff neck. Possible : Change in mental status(more extensive than meningitis pt), motor dysfunction, photophobia, fatigue, focal neuro deficits, symptoms of increased ICP, joint pain, headache, vertigo • Typical encephalitis sx • Agitation, irritability, confusion, personality changes (especially notes in herpes simplex) • Behavioral changes of encephalitis • teach families who live in mosquito filled areas to protect themselves from West Nile virus. Only swim in designated lakes and ponds. Similar interventions to meningitis. • Interventions for encephalitis • Acyclovir • Drug therapy for encephalitis • -limit time outside between dusk and dawn -wear protective clothing -use insect repellent -remove areas of standing water from flower pots, trash cans, and rain gutters -check window and door screens for holes -keep hot tubs and pools clean and properly chlorinated • Protecting family and pt from West Nile virus to prevent encephalitis • axial loading aka vertical compression • application of the forces of trauma along the axis of the spine; this often results in compression fractures of the spine. Often from falls or diving accident • spinal shock syndrome • temporary condition where pt loses motor, sensory, and reflex abilities that can last for up to 3 months after spinal injury • paraparesis • partial paralysis of the legs and lower body • L3-L5 • Hypo or hyper sensitivity to the top of the foot and Of the leg after spinal cord injury, where at is fracture • T10 • Hypo or hyper sensitivity to the umbilical area after spinal cord injury, where at is fracture • C3 or C4 • Hypo or hyper sensitivity to the clavicle after spinal cord injury, where at is fracture • C7, C8 • Hypo or hyper sensitivity to the fingers after spinal cord injury, where at is fracture • Bradycardia, hypotension, and hypothermia occur because of loss of sympathetic input. These changes may lead to cardiac dysrhythmias. systolic blood pressure below 90 requires treatment. • Cardiovascular considerations of spinal cord injury • Autonomic Dysreflexia/Hyperreflexia • A potentially life-threatening condition in which visceral and cutaneous stimuli cause a sudden massive uninhibited reflex sympathetic discharge in people with high-level SCI. Severely elevated blood pressure can cause hey hemorrhagic stroke • -A sudden significant rise in systolic and diastolic blood pressure accompanied by bradycardia. -profuse sweating above the level of lesion, especially in the face neck and shoulders. Rarely occurs below Lesion -goosebumps above or possibly below lesions -blurred vision -flushing of the skin above legion especially in neck face and shoulders, or flushing AT level of lesion with paleness below -spots in patients visual field -nasal congestion -onset of severe throbbing headache -Apprehension feeling • Signs and symptoms of autonomic dysreflexia • Assess for internal bleeding from trauma or stress ulcer. Paralytic ileus may develop within 72 hours. During the period of spinal shock, peristalsis decreases leading to a loss of bowel sounds and gastric distention and may lead to hypotonic bowel. • GI considerations for SCI • Patients with cervical or high thoracic spinal cord injuries have upper motor neuron damage that spares lower spinal reflexes causing a spastic bowel and bladder. Lower thoracic and lumbosacral injuries usually have damage to lower spinal nerves and have a flaccid B&B • What permanent GI problems occur with SCI • Prolonged immobilization can cause skin breakdown or VTE, osteopenia and osteoporosis(fracture risk). Heterotopic ossification, contractures- do ROM Orthostatic hypotension(especially cervical injuries) • Assessment of patient's for long-term complications related to spinal cord injury • Heterotopic Ossification (HO) Assess for swelling redness warmth and decreased range of motion in involved in extremities, changes in bony structure isn't seen until several weeks after sx start • Complications of spinal cord injury where there is a Creation of abnormal growth of bone in soft tissues or around joints, most common place is hip • Place hands on patient's abdomen over diaphragm and below ribs. If patient is obese put one hand on either side of rib cage. Have patient take a deep breath and cough during expiration. Assistant locks his or her elbows and pushes inward and upward as patient coughs. • Cough assist for tetraplegic • neurogenic shoc k • a state of shock (hypoperfusion) caused by nerve paralysis that sometimes develops from spinal cord injuries that will most likely occur within 24 hr and most common in pt with injury above T6 • Noxious stimuli such as full bladder, fecal impaction, wrinkle in clothing, menstrual cramps, erection, ingrown toenail, bladder infection, sitting on catheter tubing. • Autonomic Dysreflexia causes and risks • Sit pt up to decrease BP. (1st priority) Notify MD or rapid response team Assess and treat cause: check for urinary retention or catheter blockage Determine if a UTI or bladder calculi are contributing to irritation Check patient for fecal impaction or other colorectal irritation using anesthetic ointment at rectum Examine skin for new or worsening pressure injuries Monitor blood pressure every 10 to 15 minutes Give nifedipine or nitrate as prescribe to lower BP • Immediate interventions for pt with Autonomic Dysreflexia • Warn for 8 to 12 weeks and is a fixated by four pins into the outer aspect of the skull • Halo fixator for immobilization of cervical spine • -Device alters balance -wear loose clothing or large openings for head and arms. -bathe in bathtub or take sponge bath -keep as active as possible with avoiding contact sports or swimming -do not drive bc vision is impaired -use straws for drinks -cut food into small bites -before going outside in cold temps, wrap pins with cloth to prevent metal from getting cold -clean pin sites -increase fluids and fiber • Use of halo device for SCI • Tizanidine Intrathecal Bacolofen pump placed in subcutaneous pouch in lower abdomen to direct fluid into CSF Celecoxib for bony overgrowth (HO) Calcium & biphosphonates • Drugs for SCI • Sedation, fatigue, dizzy, changes in mental status. Seizures and hallucinations may occur if rapidly withdrawn from pt • Adverse effects of implanted baclofen pump • Functional Electrical Stimulation (FES) • Application of low-level, computer- controlled electric current to the muscles, including paralyzed muscles, to enhance or produce function • Men: incomplete lesions allow some control. Able to get hard from stimulation if injury above T6. Ejaculation is less predictable and may be mixed with urine. Prophylactic vasodilator May be needed before sex to prevent AD. Women: some can get pregnant, some lose ovulation , vitro fertilization May be needed. Vaginal dryness • Sexual considerations for SCI • in vitro fertilization (IVF) • egg and sperm cells are combined outside the body in a laboratory dish to facilitate fertilization • amyotrophic lateral sclerosis (ALS), effects men more than women • Uncommon Chronic idiopathic neurological disease causing progressive muscle weakness and wasting, leading to paralysis of respiratory muscles , more common in men ages 40-60 • Fatigue, muscle atrophy including tongue, muscle weakness, twitching of face and tongue, dysarthria , dysphasia, stiff and clumsy gait, abnormal reflexes • Sx of ALS • One approved drug: riluzole to slow disease Palliative psych care • Care for ALS • Guillain-Barre syndrome • autoimmune PNS condition that causes acute inflammation of the peripheral nerves in which myelin sheaths on the axons are destroyed, resulting in decreased nerve impulses, loss of reflex response, and sudden muscle weakness, effects more males than females and arrives after age 55 usually. Viral infections may trigger • Acute or initial period(1-4 wks): begins with onset of first symptoms and ends when no further deterioration occurs 2. Plateau period(lasts several days-2wks) 3. Recovery phase(gradually over 4-6 mo. And maybe even up to 2 yrs): remyelination and axon regeneration. Some pt do not completely recover and have permanent neuro deficits, referred to as chronic GBS • Three stages of GBS • Ascending symmetric weakness with decreased or loss of DTRs. Respiratory failure. Ataxia. Loss of B&B control. Paresthesia. Cramping. Facial weakness. Dysphagia. Diplopia. Difficulty speaking. Fluctuating BP. Dysrhythmias. Tachycardia or bradycardia. • Sx of GBS • Lumbar puncture to evaluate cerebrospinal fluid- high protein levels may be seen a couple weeks after disease process begins • Diagnosis of GBS • plasmapheresis or IV immunoglobulin • Tx for GBS • Do during first few days. Usually receives 3-4 tx 1-2 days apart. Weight pt before and after procedure bc edema is risk. • Plasmapheresis for GBS • -Check shunt every 2-4 hours by assessing bruit or thrill -Keep double bulldog clamps at bedside. -Observe access site for bleeding or bruising • If shunt is used for plasmapheresis, be sure to: • Citrate-induced hypocalemia Urticaria Coagulopathy depletion Risk for infection Fluid shift or depletion • Complications of plasmapheresis • myasthenia gravis • a chronic progressive autoimmune disease that affects the neuromuscular junction and acetylcholine receptors and produces serious weakness of voluntary muscles that may lead to death from respiratory failure. 2 types • Ocular Myasthenia Gravis • The muscle weakness is limited to the eyelids and extraocular muscles. One out of two types of myasthenia gravis • Generalized Myasthenia Gravis • Usually involves bulbar (extraocular, facial and muscles of mastication), and proximal limb-girdle muscles(less common) , type of MG • -Progressive muscle weakness that worsens with repetitive use and usually improves with rest -Poor posture -Ocular palsies -Ptosis; incomplete eyelid closure -diplopia -loss of B&B control -fatigue -muscle aches -paresthesias -decreased sense of smell & taste • Sx of myasthenia gravis • Pregnancy, infection, anesthesia • Onset of myasthenia gravis is usually slow. These things can cause fairly rapid development • Exposure to environmental extremes. After vaccination. Menstruation. Extreme temps. May have exacerbation. • A temporary increase in weakness may occur in MG pt because of • Cholinergic or myasthenic crisis resulting in respiratory failure or periods of exacerbation • Why is MG pt typically hospitalized • MG pt • Ask about a hx of Thymus gland tumor • Muscles of face expression, chewing, and speech are effected (bulbar involvement). Smile may turn into snarl. Chewing & swallowing difficulties can lead to weight loss. Voice becomes weaker after talking for while. Tongue gets fissures in some pt. • Bulbar sx of myasthenia gravis most pt have • Eaton-Lambert Syndrome • A form of myasthenia gravis and muscle weakness that tends to be associated with lung cancer; trunk, pelvis, and shoulders are commonly affected • Drugs to release acetylcholine, removing tumor and managing cancer, plasmapheresis or immunosuppressive agents • Tx of Eaton-Lambert Syndrome(type of MG) • Hx and physical findings. EMG. May be confirmed by pt response to cholinergic drugs. Thyroid fx should be tested bc thyrotoxicosis is present in some pt. Other autoimmune diseases may be associated with MG. • How is diagnosis of MG made • MG • Drug used for di agnosis of MG(will show marked improvement in muscle tone that lasts 4-5 min). May also be used to determine if increased weakness in already diagnosed pt is due to a cholinergic crisis(too much cholinesterase inhibitor drug) or myasthenia crisis(not enough drug). If cholinergic crisis, muscle tone won't improve and weakness will increase and muscle twitching around face may be present. • What is edrophonium for • -sx management by cholinesterase inhibitors it cholinergic drugs -helping remission by immunossuppresive agents, steroids, plasmapheresis, and thymectomy Give drugs on time ! • Tx of MG • Pyridostigmine -expect a day to day variation in dosage to manage changing sx • Cholinesterase inhibitor drug of choice for MG • Eat meals 45 min-1 hr after taking ChE inhibitors to avoid aspiration, especially important if pt has bulbar movement. Avoid meds that cause weakness. Watch for sx of cholinergic crisis. • Cholinesterase inhibitor teaching for MG pt • Assist with planning periods of rest. Assist in positioning. • Mobility promotion for MG pt • ATB May increase MG sx • ATB and MG pt • Sudden increases in weakness accompanied by hypersalivation, sweating, and increased bronchial secretions. Possible N&V&D. Life threatening sx are bronchospasm and bradycardia. Cramps. Flaccid paralysis. Miosis & blurred vision. • Cholinergic crisis sx • Myasthenia crisis • And exacerbation of MG symptoms caused by not enough anticholinesterase drugs and or caused by infection. • Increased pulse and respirations. Rise in BP. B&B incontinence. Decreased urine output. Absence of cough and swallow reflex. May often me caused by infection. • Myasthenia crisis sx • Apprehension Respiratory failure Restlessness Dyspnea Dysphagia Generalized weakness • Features common to both MG crisis and cholinergic crisis • Maintain adequate respiratory fx. May require mechanical ventilation. Anticholinesterase drugs are held bc they increase resp secretions and are ineffective first few days after crisis begins. Rest, repetitive movement can cause a crisis. • Emergency care for myasthenia crisis • Do not give anticholinesterase drugs. Atropine 1 mg IV May be given and repeated. Atropine can thicken secretion and cause airway mucous plugs. Should improve rapidly. • Emergency care for cholinergic crisis (mg pt) • -Antibodies are removed from plasma to decreased symptoms and manage exacerbation symptoms short term -6 exchanges over a 2 week period with follow up exchanges weekly or monthly as needed • Why is plasmapheresis used in MG pt and how much to use • Patient's inability to close eyes completely may lead to corneal abrasions. Eye drops and gel may help. To help relieve diplopia, cover eyes with patch for 2-3 hours at a time, one eye at a time. Pt may tape eyes shut at night • Eye considerations in MG • Watch Respiratory effort and promote gas exchange. Observe for signs of pneumothorax or hemothorax. • Thymectomy considerations for MG pt • Infection, stress, surgery, hard physical exercise, sedatives, enema. Heat. Strong laxatives. Beta blockers and antidysrhthmics, antihistamine, opioids. ATB. Alcohol. Arthritis. • Factors that increase risk for MG exacerbation • Avoid heat(hot tubs, sauna), crowds, overeating, erratic changes in sleep patterns, or emotional extremes. Teach signs of exacerbation: increased weakness, diplopia, ptosis, and problems with chewing or swallowing. Drugs normally taken before activities. Plan periods of rest. Resuscitation equipment should be in home. • MG education • -keep prescribed drugs and a glass of water at bedside if feels week in morning -wear a watch with an alarm function to remind you to take drugs -post drug schedules so others know it -keep secure supply of drugs in car or work -plans strenuous activities when the drug peaks -check with MD before using OTC drugs • Helpful hints for MG drug therapy • Trigeminal neuralgia (tic douloureux) • a condition characterized by sudden, intense, severe unilateral lightning-like pain due to an inflammation of the fifth cranial nerve and occurs more likely in women older than 50 • Classic pain: excruciating sharp bursts of pain that last from seconds to minutes Atypical pain: migraine like HA • Sx of trigeminal neuralgia • Light touch, dental procedure, changed in facial expressions, or chewing. Pt often avoids talking, smiling, eating, or hygienic needs out of fear. • Trigeminal neuralgia pain triggers • Drug of choice is carbamazepine. Gabapentin, pregabalin, and baclofen can be used. Acupuncture • Drugs for trigeminal neuralgia • Microvascular decompression radiosurgery nerve block • Surgery used for trigeminal neuralgia when drug don't work. • percutaneous stereotactic rhizotomy • Surgical treatment for trigeminal neuralgia where surgeon passes a hollow needle through the inside of patients cheek into the trigeminal nerve fibers and a heating current (radio frequency thermocoagulation) goes through the needle to destroy some of the fibers. A glycerol injection may also be used but is not done as commonly as thermocoagulation. Under general anesthesia • Apply ice pack to site in cheek and jaw for 3-4 hr. Assess if nerve damage was done. Discourage pt from chewing on affected side until Paresthesias resolve. Soft diet prescribed. Avoid rubbing eye on affected side bc can no longer feel pain and tell if injury has occurred. Inspect eye daily and report redness or blurry vision. Stress importance of regular dental check ups bc absence of pain. • percutaneous stereotactic rhizotomy post op care and teaching. • Microvascular decompression • Surgery for trigeminal neuralgia where artery compressing the nerve is relocated, requires craniotomy • Bell's Palsy(facial paralysis) aka cranial polyneuritis • temporary paralysis for 2-5 days of the seventh cranial nerve that causes paralysis only on the affected side of the face most commonly occurring in young adults and ppl w DM • Pain behind ear or on face may occur a few hours or days before paralysis. Paralysis of facial muscles on affected side. Pt can't close eye, wrinkle forehead, smile, whistle, or grimace. Tearing may stop or be excessive. Face is masklike and sags. Impaired taste. Tinnitus. Most pt go into remission within 3 mo. • Bell's palsy sx • Believed to be result of inflammation triggered by herpes simplex virus. Infection, altered immunity, or exposure to cold may trigger virus activation. • What is the cause of Bell's palsy • 30-60 mg corticosteroids daily during the first week of onset of sx. Antivirals for 7-10 days after sx begin. Mild analgesics. Chronic- Gabapentin • Medical management for Bell's palsy • Bc Eye doesn't close, watch for abrasions. Teach to manually close eye at intervals and use eye drops. May be patched or taped at bedtime. May be unable to chew, sip through straw, or control drool on affected side, creating difficult meal times. Eat and drink using unaffected side. Eat high calorie snacks. Soft diet. Practice using face muscles 3-4 times daily for 5 min each. • Teaching for Bell's palsy • dermal appendages • sweat and oil glands and hair follicles • Skin can regrow when epidermis is damaged but cannot regrow when all of dermis is damaged. Partial thickness burns reduce the activation of vitamin D and this function is lost completely in full thickness burns • When can a burn injury no longer be restored by own skin • Superficial-thickness wounds, partial-thickness wounds, full-thickness wounds, and deep full-thickness wounds Also classified as minor moderate or major. • Classifications of burns (4) • Superficial thickness burn • Only epidermis is damaged. Sun burn is classified as what? • Mild edema and redness. Alteration in comfort. Increased sensitivity to heat. Desquamation occurs 2-3 days after burn. Heals in 3-6 days.