MEDSURG EXAM 3

intercranial pressure (essentail colume components and %) (3)

brain matter → most 78% 12%→ blood in arterial, venous and capillary 10% is the CSF

Immunodialators examples (3) and how injected?

interferon B-1a (rebif, Plegrdy, Avonex)--> IM interferon B-1b (Betaseron, Extavia)--> sq Glatiramer acetate (Copaxone, Glatopa)--> SQ

autoregulation

is the automatic adjustment in the diameter of the cerebral blood vessels in the brain to maintain constant blood flow during chnage sin BP

hyperesthesia

**sometimes have hieghtened sensitivity right above the lesion because not completely transected -

Genetic Link of PD

-approx. 15% have a fam hx many autosomal dominant and recessive have been linked

Summary of major S/S of IICP -early

Early: change in LOC and confusion**

s/s of concussion -physical

HA Nausea Vomit Incoordination Dizziness Visual Problems Fatigue Photopia (light) Phonophobia (sound)

Nursing DX for TPA

#1 risk for bleeding #1 impaired mobility and communication

MRI (stroke diagnostic)

More effective in identifying ischemic stroke→ MOST EFFECTIVE BUT TAKES LONG Takes longer to completed → 1-2 hours to be completed and may have to wait for one

Secondary progressive MS

begins as relapsing-remitting then becoming steadily progressive tend to form from RRMS RRMS phase and then SPMS

Assessing Pronator Drift

Evaluates upper motor strength PT sitting or standing and put arms up with palms up → have them close eyes if left sided → pronate right arm downwards usually not both sides because that means they ahve had a really devastating stroke

bilateral dilated pupils

→ midbrain injury

Drug Therapy LEVADOPA-CARDOPA * ther name * levodopa --> what is it and what does it do // when *Cardopa --> what is it and what does it do * result of this combination * hjow do you take * when do take

(SINEMET) → often FIRST drug used precursor of DA and crosses blood-brain barrier; converted to DA in the basal ganglia Carbidopa inhibits an enzyme that breaks down levodopa before it reaches the brain levodopa is converted to DOPAMINE in the brain Carbidopa helps prevents the breakdown of LEVODOPA before it can reach the brain and take effect RESULT OF THIS DRUG --> combination is more levodopa can reach the brain and less drug is needed SINIMET : it is a Carbidopa that helps Levodopa to reach to the brain PO medication and should be taken at least an hour before or two hours after food in empty stomach needs to be taken on a regular basis to help with symptoms management needs to be on regular regimen→ necessary to help them function

Tensilon Test

(edrophonium chloride) It is an anticholinesterase agent that blocks the enzyme acetylcholinesterase→ the enzyme that breaks down Ach. --> reveals imporved muscle contractility after IV injection of endrophonium chloride --> this test also aids in the confirmation of cholinergic crisis

IMPACT → management model for concussion

(important to not send them back into game) Step 1 → Preseason and baseline testing and education Step 2→ Concussion is suspected Step 3 → Post injury testing and tx plan Step 4 → is athlete ready for non-contact activity Step 5 → determining safe return to play

AMERICAN ACADEMY OF CONCUSSION SEVERITY -grade 1 -grade 2 -grade 3

* Grade 1: Transient confusion, no loss of consciousness. Mental status abnormalities detected on examination resolve within 15 minutes. * Grade 2: Transient confusion, no loss of consciousness, signs and symptoms on examination last more than 15 minutes. * Grade 3: Any loss of consciousness, whether brief (seconds) or prolonged.8

COMPLICATIONS OF ICP ***DIABETES INSIPIDUS -what happens -tx --what solution and why -what drug is it called -limit what drug

* Urinating a whole lot// high chance for dehydration Correct underlying cause (can put pressure on hypothalamus or pituitary) Fluid replacement with IV hypotonic solutions → we want them to hold onto fluids now IV Vasopressin (DDAVP) → synthetic ADH → can give IV Consider other meds patient is on! Esp. if on mannitol → this will make them also dry and dehydrated -_> we need to limit our mannitol Ask them about which hormone is affected - they had DI and SIADH in patho - make them think about what happens in both DI most common in TBI, may see SIADH more often with brain tumors May need to stop Mannitol or increase IV rate Think about fluid volume deficit and fluid and electrolytes

Anticoagulation therapy for VTE PROPHYLAXIS -at moderate risk who is not bleeding (3) * at low risk * at high risk

* for a hospital medical patient at risk for thrombosis who is not bleeding: UH, LMWH, or fondaparinux *for a pt at low risk -anticoagulation therapy is not needed *high risk (trauma) UH or LMWH

CASE STUDY...Your patient is gradually being weaned from the vent. You are suctioning him when the heart monitor alarms sound. You notice his cardiac rhythm. WHAT OTHER INFORMATION WOULD YOU NEED TO APPROPRIATELY HANDLE THIS SITUATION?

* he is in sinus bradycardia * look at pulse ox // bp WHAT WOULD YOU DO FIRST??? * put him back on the vent and give o2 if that doesnt work --> call code

Spasticity Treatment

* heat passive ROM electrical stimulation meds --> BACLOFEN TIZIDINE, DANTRIUM--> inhibit transmission of impulses fromSC to muscles medical marijuana surgery (cordotomy, rhizotomy)

Diagnostics of PD -confirmation of disorder

* no specific diagnosis of PD * clinical diagnosis requires the symptoms of TRAP and a asymmetric onset CONFIRMATION: positive response to antiparkinson drugs (levadopa and dopamine agonist) no MRI or CT--> can rule out other stuff tho

MANNITOL (osmitrol) -type of drug -how you five it -onset -major side effect -key point of assesment

**** (50 ml glass container → need a filtered needle b/c can get crystals) Osmotic diuretic → give through filtered needle → hypertonic solution Rapid onset → within 15 minutes *** Major side effect → dehydration Key point of assessment → urine output, overall I&O, serum osmolarity Can become dehydrated

VTE DIAGNOSTIC STUDIES

Lab work: PTT, PT, INR, Hgb, Hct, Platelet count, and D-dimer Noninvasive venous study Venous duplex ultrasound Invasive (rarely formed) Computed tomography Contrast venography (Phlebogram)

DRUG THERAPY --> FACTOR X INHIBITORS * examples 2 major * how administered * rapid *antidote *action

*Rivaroxaban (Xarelto)* *Apizaban (Eliquis)* fondaparinux (Arixtra) Edoxaban (Savaysa) Administered Orally Rapid onset Antidote : Andexanet Alfa (andexxa)* (FDA approval 2019) ACTION: inhibit factor X (directly or indirectly) producing rapid anticoagulation

CASE STUDY...You notice that your patient's skin is very cold. His temp is 35.9 C. You recall that poikolothermia is common in quads. Poikolothermia: -def -pt teaching -nursing tx

*SNS interruption prevents peripheral temperature sensations from reaching hypothalamus; ↓ shivering and sweating --> outside cold hypothalamus is not detecting it *Assume temperature of the environment--> at risk for both hyperthemria and hypothermia *Dress appropriate to environment *Warm fluids vs cooling blanket nurisng dx: altered thermo regulation knowledege deficieny --> look at weather

compression of cranial nerve 3

-oculomotor nerve, results in dilation of the pupil in the ipsilateral side of the lesion -sluggish no response to lgoht, inability to move eye upward or abduct, caused by brain shifting

Indirect thrombin inhibitors --> UNFRACTIONATED HEPARIN (HEPARIN) * how its given * what lab is important (normal and with therapy) * Antidote * ACTION

*GIVE IV (Therapeutic)--> there is a clot there *orGIVE SQ (Prophylaxis)--> preventing clots from forming ******IN CLINICAL SEE 5,000 UNITS SQ BID → PROPHYLACTIC ******HEPARIN INFUSION → PROBS CLOT SOMEHWhere **Labs : PTT (IV hep usually) normal 25-35 therapeutic 2x normal → IV **Heparin effects the intrinsic common pathways of blood coagulation by antithrombin → look at the blood cascade when looking at thrombin ----> inhibits thrombin mediated conversion of fibrinogen to fibrin **Antidote → Protamine Sulfate

SPINAL SHOCK * happens when *last how long * what does it cause (s/s) * how many people get

*impingment of spinal cord Happens within 1st hour of injury Duration 1-6 weeks Temporary neurologic syndrome Characterized by -↓ reflexes -Loss of sensation -Flaccid paralysis below level of injury Experienced by about 50% of people with acute spinal cord injury This syndrome lasts days to months and may mask postinjury neurologic function. Active rehabilitation may begin in the presence of spinal shock.

Indirect thrombin inhibitors --> LOW MOLECULAR WEIGHT HEPARIN (Enoxaprin-Lovenox) * differences from heparin * how do you give * what about the dose * Labs * Antidote * main SE * PT education

*more bioavailability, more predictable dosing, longer half-life, few complications (bleeding) * less likely to cause HIT and osteoporosis give SQ **--> do not expel air bubbles before given prophylactic (standing 40 mg SQ daily) or Therapeutic (weight based dosage) look at label to see what dose giving don't trust the package it comes in b/c sometimes package doesn't always match *LABS: not required but need to look at Creatine metabolized by the kidneys therefore if kidney dysfunction→ not want to be on it (build up quicker) * Antidote : Protamine Sulfate (partly reverses) main SE: bleeding PT Education: important because going home on this med need to be comfortable giving themselves this SQ injection milk carton → to put needles in and bring to drs office to dispose needles

Halo Vest --> CARE

- can wash hair -position with pillows to make comfy * if you undo bottom part of vest --> can perform CPR * can be liften up and side to side

DIAGNOSIS of SCI?? ASIA --> american spinal injury of association

--> how we diagnose complete --> means no motory or sensory function normal --> good incomplete --> either sensory or motor effective no need to study or memorize but a--> is the worst e is th enormal

HIRUDIN and ARGATROBAN

->very rarely given usually only under guidelines of a hematologists * these are used as an alternative to heparin for prevention and tx of HIT

Stroke Code

Patient identified to meet criteria for acute stroke and decision made to administer IV t-PA. alerts ICU that they are getting a pt, gets the team ready to amke things go faster and smoother

MS DRUG THERAPY SIDE EFFECTS

-Flu like symptoms fever, night sweats and muscle aches are main side effects. -Liver toxicity in some patients. -Considerations: depression, suicidal ideation possible→ BLACK BOX warning -Wear sunscreen and protect from sun (photosensitivity) → pt education: sunscreen, protect when go out -Rotate injection site with each dose -Infusion many serious side effects

Complications of VTE

-PE -chronic thromboembolic pul. HTN -post-thrombotic syndrome (from chronic venous HTN that results in vein and valve damage) -phlegmasia cerulea dulens (rare --> happens with cancer pts, need to be treated b/c gangrene and amputation)

OTHER DRUGS **AMANTADINE

-antiviral agent -weak anatagonist of the NMDA-type glutamate receptors, increases dopamine release and blocks dopamine reuptake -provides only mild relief and seldom used in early stages of PD -extended therapy can worsen dyskinesia

Non-motor symptoms of PD

-depression, anxiety, apathy -fatigue, pain -urinary retention and constipation -erectile dysfunction -sleeping problems (trouble staying alseep at night and nightmares during the REM sleep seen in pre parkinson

ASSISTIVE DEVICES

-easier for them to use to eat --> helps prevent it from sliding off the face * cups may have different handles etc--> helps them have some levels of independence

DA as a neurotransmitter

-essential for functioning of the extrapyridimal motor system --> including control of posture, support and voluntary motion

V/Q Scan

-if the patient cannot have contrast media and has two components 1. perfusion: injection of radioisotope and scan 2. ventilation inhalation of radioactive gas and scan; need patient to be cooperative and inhale → sometimes this is part of the problem if not able inhale low/med/high risk

NURSING MANAGEMENT --> DRUG THERAPY

-patient and family teaching for anticoagulation -mechanism of action/length of therapy -same time of day (afternoon/evening best) -must do blood test follow-ups with local MD -Notify of adverse effects -when to call dr, go to er -severe ha (some type of bleeding in brain), blood in urine, stool, vomiting blood, chest pain dizziness -stomach pain → gastritis etc -avoid trauma or injury that causes bleeding -avoid aspirin and NSAIDs→ they have some antiplatelets mechanisms Aspirin → antiplatelet → does not let them aggragate which can cause further bleeding wear medical alert bracelet → should indicate on blood thinner and emergency contact -limit alcohol -avoid changes in eating habits (like leafy green veggies) → have VK -avoid herbal products unless approved by physician can interact with → after dvt and mobilizes

Postural Instability

-patients may complain of not being able to stop themselves form going forward (propulsion) and backwards (retropulsion) to test --> examiner stands behind the pt and tug backward on the shoulders causing the pt to lose balance and fall backwards

PE interprofressional CARE

-prveention starts with the prevention of a VTE--> if a PE is suspected start the tx right away HOB elevated helps WOB oxygen → if hypoxic start with nasal cannula or mask (venturi/nonrebreather) intubation and mechanical ventilation if ABGs indicate or if breathing 50 min and pulse ox so low pulmonary hygiene → cough and deep breathing, IS , OOB shock: IV fluids and/or vasopressors Heart Failure Diuretics

Nursing diagnosis

-risk for ineffective airway clearance -possible impaired gas exchange -decrease cardiac output -immpaired mobility

Spinal Fusion

-should not go into an MRI

ventriculostomy

-specialized catheter is inserted into the lateral ventricle and coupled to a external tranducer -measures pressure within ventricles, facilitates removal and sampling of CSF, and drug therapy -should be level with the foramen of Monroe and tragus of the ear

TIA carotid system involvement S/S

-temporary loss of vision in one eye (amaurosis fugax) transient hemiparesis numbness or loss of sensation sudden inability to speak

Thrombotic Stroke -type of stroke -what happens -most common in who and what disease -preceded by what -in first 24 hours do not have what -how long does it take the symtpoms to manifest

-type of ischemic stroke Most common (60%) the artery that normally supplies the blood to it gets blocked → blood flow is reduced or completely stops usually due to plaque (similar to PAD → something in there starts to form and artery gets blocked) most common in older individuals --> esp. in those with high cholesterol, athersclerosis, or DM -most commonly associated with HTN and DM --> both which accelerate athersclerosis -many times preceded by a TIA -extent of stroke is dependent on: ---onset, size, collateral circulation ---most pts with ischemic stroke do NOT have decrease level of consciousness in first 24 hours unless brainstem stroke or other conditions -manis progress in first 72 hours as infarction and cerebral edema increase

motor strength

0 Unable to lift the arm or leg to command, or in response to painful stimuli 1→ Flicker of movement is felt or seen in the muscle(s) of the limb 2→ Moves the limb, but unable to raise the extremity off the bed 3 → Able to lift the extremity off the bed briefly, but does not have the strength to maintain the lift 4 → Able to lift the extremity off the bed, but has difficulty resisting the examiner ("I am going to push your right arm/leg down, so try to prevent me from doing that") 5 → Able to lift the extremity off the bed and maintain the position against resistance Always know to do side to side so you can compare

NIHSS stroke severity score

0→ no stroke symptoms 0-4→ minor stroke 5-15→ moderate 16-20→ moderate to severe 21-42 → severe

HVIS stroke code

Patient identified to meet criteria for acute stroke and decision made to have a neurointerventional procedure performed

normal Compensatory adaptations for ICP

1. Autoregulation - cerebral vessels change size 2. CHANGES IN CSF VOLUME--> CSF - decrease production or shunt more CSF down spine 3. Brain tissue displaces (but if too far - herniate!)--> distention of dura or compresion of brain tissue

Dysreflexia -who is affected

1. dysruption of autonomic reflexes following spinal injruy -no connection from stimulus to autonomic nervous system to brainth T6 or above stimulus may be full bladder or constipation or impacted --> this stimulus causes massive sympathetic response below the level of the lesion--> wide spread vasoconstriction --> HYPERTENSION --> causes baroreceptors tp detect this and slow hr --> should help inhibit HTN but because it is blocked there is an abnormal --> only for those with spinal cord lesions wi

VIRCHOW'S TRIAD

1. endothelial injury→ 2. abnormal Blood Flow 3. Hypercoagulability

Impaired physical mobility --> FOR FREEZING

for freezing rock from side to side conscious thought about stepping over real/imaginary lines drop rice kernas, step over Lift toes when stepping take one step backward and two steps forward

PD --> surgical options 3 types

3 categories 1. Deep brain stimulation is reversible, shown to control symptoms better improve motor function, decrease dyskinesthia 2. Ablation (destruction of areas of the brain that affected by PD 3. Transplantation--> of fetal neural tissue in the ganglia designed to produce DA - producing cells

normal ICP values -when considered IICP?

5-15 mm Hg - once you are above 20 mm Hg - considered to have increased ICP (IICP)

STROKE # cause of death -other names -how many people

5th most common cause of death in the United States other terms: -Brain attack -Cerebrovascular accident (CVA) ~7 million people over the age of 20 have had a stroke ~34% of strokes occur less than 65 years old 15-30% of people have a permanent disability--> why onset medical attention is crucial Occurs when there is ischemia (inadequate blood flow) or Hemorrhage (bleeding into the brain) depending on severity and location (can lose functions such as movement, sensation, thinking, talking, or emotions that are controlled by the affected area

NIHSS national institute of health stroke scale -how many questions -what is the scoring and what doe sit mean -who adminsters -what is it predicting / looking for -what is it evaluating

A 15-item neurological examination used to evaluate the effect of an acute stroke Score ranges from 0-42 Predictor of both short- and long-term outcomes **have to be trained to administer **look to see how th epts perform activites and answer questions Evaluate the effect of acute cerebral infarction on the levels of: consciousness language neglect--> stand on right side and not responding visual-field loss extraocular movement motor strength ataxia dysarthria sensory loss (including cranial nerves) score of 0--> no stroke 42--> devastating stroke takes about 10 minutes

A 50-year-old presents with signs of a stroke. What is the priority interventions?

ABCs! Pulse ox!!!!!!!! -may have a difficult air way and not be able to support b/c unconcious -pts usually become worsen within 24-48 hours--> can't always go with baseline Oxygen, intubation, and mechanical ventilation if necessary Call Stroke Team Transfer to certified stroke center--> not all facilities have these Perform baseline neuro assessment -level of conciousness, sensation, speech, orientation IV access (18 g)--> larger better EKG Non-contrast CT scan--> within 20 mintues

SCI --> INITIAL PRIORITIES

AIRWAY AND SPINE IMMOBILIZATION spinal cord injury → always thinking about spine mobilization → you are not going to hyperextend the neck but instead do a JAW THRUST→ push jaw forward and opens the airway * always immobilize spine BREATHING & OXYGENATION--> rescue breathing if possible CIRCULATION & CARDIOVASCULAR STABILITY--> can cardiac arrest Prevent extension of cord damage--> IMMOBILIZE SPINE

WEIGHT SHIFTS

AKA "PRESSURE RELEASES"--> high risk for altered skin integrity and skin ulcers TILT CHAIR BACKWARDS LATERALLY SHIFT USING ARMS PUSH UP FROM BUTTOCKS USING ARMS WHY ARE SPINAL CORD INJURY PATIENTS PRONE TO SKIN BREAKDOWN, OSTEOPOROSIS, & DVTs? * because dont have feelings Osteoporosis--> no weight bearing DVT--> not moving well

CLINICAL MANIS -affect -intellectual (rihgt/left)

Affect Emotion control→ esp. if in frontal lobe (where emotions are) Wide range Intellectual Function Memory judgement Right-side Impulsive Left-side Move slowly and cautiously

Types of Hemorrhagic Stroke -AVM vs ANEURYSM - ____ and ____ (the other two categories)

AVM → blood passes quickly from artery to vein bypassing the usual capillary system, any of these vessels can rupture which causes bleeding in the brain Aneurysm→ a ballooning or weakened area of the blood vessel--> if left untreated the aneurysm will continue to weaken until it ruptures and bleeds into the brain intracerebral and subarachnoid hemorrhage in the pons is the most serious because basic life functions

Myasthenia Crisis -triggers -major complication -what is important to have at the bedside

Acute worsening of muscle weakness triggered by: Respiratory infection Surgery Emotional Distress Pregnancy Medications Beginning Treatment with Corticosteroids → tx is this but can also cause crisis MAJOR COMPLICIATIONS swallowing // breathing → aspiration, respiratory insuffiency, URI what is important to have at the bedside suction equipment oxygen ambubag

REHABILITATION -after the acute phase * after what amount of time

After stroke has stabilized for 12 to 24 hours, collaborative care shifts from preserving life to lessening disability and attaining optimal functioning. Average length of hospital stay 5.3 days Patient may be transferred to a rehabilitation unit, outpatient therapy, or home care-based rehabilitation. Goals: prevent deformity, maintain and improve function--> dont wnat contractures or atrophy of muscles Interdisciplinary team: RN, MD, pharmacist, social worker, psychiatrist, chaplain, dietitian, and therapists in PT, OT, RT, speech, vocation, recreation Max benefit in first year!!! The rehabilitation nurse assesses the patient and family Rehabilitation potential of the patient Physical status of all body systems Presence of complications caused by the stroke or other chronic conditions Cognitive status of the patient Family resources and support--> imperative Expectations of the patient and family related to the rehabilitation program

NON-MODIFIABLE RISK FACTORS

Age→ increases with age greater than 65 Gender→ more men have stroke mor women die Ethnicity → AA have 2x incident (may be from the underlying conditions) Family History--> genes putting people at risk for thrombosis, lipids, amd vascualr diseases

IMPAIRED VERBAL COMMUNICATION

Allow time to communicate Encourage deep breaths before speaking Provide alternative means of communication flash cards Communication boards→ can point Consult speech therapy

HALO-BRACE * def * allows for what * duration * what is done to confirm correct position

Allows more mobility and better able to begin rehab May be used after surgery until fusion healed Causes less pain 8-12 week duration X-ray confirms correct spine position after application -temporarily measure that is applied to heal bony problem

Myasthenia Gravis --> PATHO * antibodies destroy what

Antibodies destroy the acetylcholine (ACh) receptors decreased numbers of ACh receptor sites at neuromuscular junction Prevents ACh molecules from attaching to receptors and stimulating muscle contraction - thus weakness results Adequate supply of ACh but no effective nerve impulse transmission to muscle blocked receptor sites -blue acetylcholine pink is receptors → for some reason these antibodies prevents transmission and doesn't allow contraction → acetylcholine supply is normal but they won't connect to the receptors antibody occurance is seen in 90%

Other agents to manage PD * anticholinergics * antihistamines

Anticholinergics↓ activity of acetylcholine - benztropine (Cogentin) Antihistamines with anticholinergic or β-adrenergic blockers are used to manage tremors.

MG --> DRUG THERAPY * class of drugs * most common * action * onset of action// peak// duration * dosage * when to take * SE

Anticholinesterase inhibitors drugs * Pyridostigmine (Mestinon)** MOST COMMON Acetylcholinesterase is the enzyme that breaks down ACh - thus inhibiting this enzyme by anticholinesterase inhibitor will prolong action of Ach and facilitate transmission of neuromuscular junction impulses Rapid onset of action (15 to 30 minutes) with peak action at about two hours its effects last for three to four hours, sometimes longer Dosage: every six hours or three times a day; others need a dose every three hours to maintain symptomatic benefit. May take 30-60 minutes before meal to promote effective swallowing SE→ abdominal pain, diarrhea and increase in secretion maintenance is imperative → need stable measures → time is very important → may need to keep a diary to document when they took the medication and when the symptoms started to develop

PE --> DRUG THERAPY

Anticoagulants: SQ low-molecular weight heparin -Enoxaparin-Lovenox -What is important to know? -give therapeutic dosing → weight based drug Heparin infusion PTT while on these → when we will start these drugs Warfarin (Coumadin) INR turn off heparin infusion until INR is adequate Apixaban (Eliquis), Dabigatran (Pradaxa) Fibrinolytic agents -Tissue plasminogen activator (tPA)--> neuro q 15 x4→ very time intesive - Alteplase IV push→ for major PE, increases VS, neurochecks monitor for s/s of bleeding cannot give this if recent ichemia stroke

DRUG THERAPY --> interprofessional care

Antiplatelet: ASA, Ticlopidine (Ticlid), clopidogrel (Plavix)--> most common to go home onDipyridamole (Persantine), Persantine & ASA (Aggrenox) Anticoagulation: Coumadin, Xarelto, Pradaxa, Eliquis for those with documented atrial fibrillation (or if afib have they been taking this0 LDL control - <100 (< 70 if multiple risks) Statin (simvastatin, lovastatin) → if lipids are not controlled

Nursing Interventions CONTROL METABOLIC RATE -why is this important -what do we need to look for

Any thing that increases metabolic rate will also increase ICP **Maintain normothermia → standing order for tylenol to keep them normo ***Prevent seizures→ invasive injury or blood in CSF, may need to also give meds (ativan lorazepam, phenytoin) (side rails) (suction) When they do have seizure side lying position with rails up ***Control blood sugar Accuchecks q 6 hours with sliding scale insulin **Control pain and anxiety May be getting narcotics (short-acting) that can be reverse with narcan ***Neuromuscular blockers → cisatracurium Completely stop their movement (someone who postures or seizures a lot) Sedatives → Propofol (Diprivan)

VITAL SIGNS ASSESSMENT -as ICP rises what also rises -HR is _____ related to ICP -Cushings triad

As ICP rises, so does BP to maintain CPP; avoid hypotension to prevent cerebral ischemia HR is inversely related to ICP - treat bradycardia < 40-50 Cushing's Triad: increased SYSTOLIC BP with widened pulse pressure, bradycardia with bounding pulse, irregular Respirations*******

AVOID INCREASED INTRATHORACIC & INTRA_ABDOMINAL PRESSURE

Avoid Valsalva & isometric exercise When do people do this → hold breathe or making a bowel movement (why on stool softeners) Minimize sneezing coughing, blowing nose May need to instruct patient if awake and able to understand May use cough suppressants, stool softeners, antihistamines→ in order to decrease the pressure

CLINICAL MANIS --> respiratory system

Cervical and thoracic injuries cause paralysis of * abdominal muscles * intercostal muscles Pt cannot cough properly * Leads to atelectasis or pneumonia (may be breathing ok but not clearing) pneumonia --> high cause of death for these pts

ACUTE. CARE -bladder retraining

Bladder retraining Adequate fluid intake Keep fluid intake between the hours of 7:00 am to 7:00 pm--> so not having to get up at night Scheduled toileting every 2 hours--> like a toddler Observing for signs of restlessness--> can be a sign their bladder is full. but not know they need to empty Assessing post void residual--> how much urine in bladder after voiding

CASE STUDY...Your patient's urinary output has been adequate. Because of the level of injury, he has a spastic bladder. He is on an intermittent catheterization schedule. He is taught to limit calcium in his diet to 1g/day and drink about 2L fluid/day. NEUROGENIC BLADDER *what do we do as nurse --> implementations

Bladder retraining, intermittent catheterization (4-6 x/daily), external catheter, or indwelling catheter * set alarm to go Dependent on type of location of lesion, UE function, caregiver burden, lifestyle choices May need meds to relax muscles or to contract bladder, e.g., oxbutynin Surgical diversion if repeated stones or UTIs Lewis et al. 2018, p. 1360, also Table 60-9, p. 1433

PE DIAGNOSTIC TESTS -imagaing

Chest X-ray quick and easy ruling out other disease processes EKG may see sinus tachy right heart strain → may see changes in the T wave Echocardiogram ultrasound of heart → looking for right heart strain CT angiography (CTA)** V/Q svan

Peripheral Venous Disease : CHRONIC

Chronic Venous Insufficiency (CVI) Venous Ulcers

GBS --> collaborative care --> respiratory

COLLABORATIVE CARE respiratory monitor forced vital capacity (FVC) if <15ml/kg or 800 ml, consider intubation/vent Monitor negative Inspiratory Force (NIF) <60 cmH2O → consider intubation markers for respiratory failure Monitor ABGs Suction PRN Chest physiotherapy → so no infections Watch for Infection

GBS Complications

COMPLICATIONS monitor for the high possibility of respiratory failure as paralysis progresses (30% of patients) URIs/UTIs Paralytic Ileus Muscle Atrophy DVT/PE SKin Breakdown → immobile Orthostatic Hypotension→ nervous system malfunctions Nutritional Deficiencies Electrolyte and fluid shifts associated with SIADH

Key Diagnostics -what do you not do

CT Scan (without contrast)--> b/c takes to long to get contrast → want to move fast with these Labs CBC, electrolytes, BUN, creatinine, PT/PTT/INR, glucose(s/s of neuro may be hypoglycemia)--> think about bleeding and white count May get serum osmo in anticipation of giving Mannitol IV MRI TRANSCRANIAL DOPPLER → cerebral artery problems clots etc CEREBRAL ARTERIOGRAM → dye NO LUMBAR PUNCTURE→ (spinal tap)this would potentially release the pressure in the brain→ it may make the brain herniate downward very bad

ACUTE CARE -cardiovascular system

Cardiovascular system Goal to maintain homeostasis Nursing goals: Monitor vital signs HTN--> depending on intervention like TPA --> may want higher Monitor cardiac rhythms Monitor I and O

THROMBOLYTIC THERAPY FOR VTE TREATMENT * how is it administrated * 2 examples of these drugs *action

Cathether directed administration of a thrombolytic drugs Urokinase tPA (altapse) will dissolve the clot and reduce the acute symptoms → use x-ray imaging and a cath to guide and out into clot and the medication is then release (and may viabrated) to break up and get rid of the blockage) Low risk for bleeding with an acute, extensive, symptomatic proximal VTE but still at risk Will need systemic anticoagulation just can't do this alone → need sometype of anticoagulant

MS MANIS -other * think cerebellar * mouth * emotional * over all tired * cognitive

Cerebellar dizzy, vertigo, loss of balance, intentional tremor, Nystagmus Dysphagia → risk for aspiration, can they swallow may have feeding tubes Fatigue from medication, sometimes environment like high humidity Emotional anger, depression, euphoria → range of emotions Cognitive about 50% experience problems with short-term memory attention word finding info processing Intellect unchanged **(more of just cognitive)

ICP etiology (6)

Cerebral Edema Concussion Contusion Hematoma Hydrocephalus Tumor

COMPLICATION cerebral vasospasm * common after what * onset // days in ICO * management of what with what specific drug * TCD??

Cerebral Vasospasm (30-70%)--> VERY COMMON AFTER SUBARACHNOID HEMORRHAGE prolonged but irriversible narrowung of cerebral arteries that begins days after cerebral hemorhhage occur in circile of willis Onset 3-5 days, max 21 days (peaks 7-10 days) 21 days in ICU → because this risk is so common Blood Pressure management Oral Nimodipine 60 mg every 4 hours (Ca channel blocker)--> restricts influx of calcium ions into the cell and reducing numbe rof open calcium channels -_> VERY PARTICULAR DRUG (dont know why this helps so much Induced hypertension→ b/c dont want cerebral perfusion pressure to go too low Transcranial Doppler (TCD)--> non-invasive method to measure vessel diameter and blood flow→ if you see a change indicates

Cerebral perfusion Pressure -def -equation -normal values vs ischemic death

Cerebral perfusion pressure reflects blood flow to brain CPP=MAP(mean arterial pressure → can take right off monitor) - ICP**** normal value 60-100 mm Hg ischemia/death < 50 mm Hg CPP → shows us getting enough o2 and nutrients to the brain → want 60 or above

Parkinson's Disease -def charcaterized by what -increase wiht what -over what age -who is more likely

Chronic, progressive neurodegenerative disorder Bradykinesia→ slowness, retention in movement Rigidity→ decrease muscle tone Tremor at rest Gait changes Increase with age Over the age of 50 Males are 1.5 times more likely to have PD

TYPES OF MS (4)

Clinically Isolated Syndrome (CIS) Relapsing-Remitting (RRMS) Primary Progressive (PPMS) Secondary Progressive (SPMS)

CLINICLA MANIS -communication * look over recpetive and expressive and glocal *dysarthia

Communication Left hemisphere is dominant for language skills in right-handed persons and most left-handed people*** Aphasia/dysphasia Receptive--> loss of comprhension Expressive-_> inability to produce language Global--> total inability Dysarthria--> muscular//mechanics of speech Treat patient as an adult Present one idea at a time***--> going through a lot present ideas differently Talk slowly, clearly, with a normal volume and tone--> not death Use simple words Encourage gestures, writing, drawing if unable to get point across verbally--> writing sometimes is very difficult // aybe use a communication board Allow person plenty of time to speak--> in brain it makes sens ebut may take them awhile

Sexual Dysfunctioning

Complete UMN: reflexogenic erections; orgasm & ejaculation not possible Complete LMN: neither reflexogenic nor psychogenic Women remain fertile but with 50% experiencing orgasm; can have vaginal delivery Men - poor sperm quality but prognosis improving to father children Incomplete lesions may vary; may have psychogenic erection & ejaculation

VTE DIAGNOSTIC TEST -Invasive (rarely performed) *CT *Contrast venography (phlebogram *MRI

Computed tomography (CT)--> uses spiral CT to evaluate veins in pelvis thighs and calves after contrast material Contrast venography (phlebogram) not seen often // typically go to ultrasound --> X-ray determination to determine location and extent of the clot, identifies collateral circulation MRI --> can be done with or without contrast evaluates blood flow through the veins, can distinguish between chronic and acute (not good with calf veins)

ORGAN DONATION

Consider cultural and religious beliefs Consider suddenness of situation Consider age of patient Consider myths of organ donation Consult "Gift of Life" expert to approach family about donation→ more positive response when use this → this helps b/c usually brain death is sudden and we need a good communicator Maintaining organ perfusion and function until taken for organ harvesting→ a whole team performs this → important to remain good perfusion → go to the OR looking alive Family support and follow-up- be sure you have made your desires known to family and friends and vice versa; living will, healthcare proxy, etc.

IMBALANCED NUTRITION LESS THAN BODY REQUIREMENTS and IMPAIRED SWALLOWING

Consult speech therapy and nutritionist Risk for aspiration - Maintain upright position for meals, bite sized pieces and/or soft and thick liquid diet→ no diet (ex→ no water if on thick diet Six small meals/day less exhausting; allow adequate time to eat less exhausting Adequate roughage and fruit to prevent constipation Have suction available Levodopa absorption impaired by protein and vitamin B6 - sometimes advised to limit protein intake until evening meal

ICP DEVICES

Continuous assessment of patient's response to environment→ put right into the brian Assess effectiveness of treatment Drain CSF (Intraventricular catheter only!) → some of them drain Intraventricular cath→ was talked about also with peds → hydrocephalus

Rotorest Bed - Kinetic Therapy kin bed -def -why does it help -nursing dx

Continuous side to side rotation at 40 degrees or more Decreases pulmonary complications Redistributes pressure to reduce pressure ulcers Can use traction pt is placed in this device, pads that come out closely to limbs to keep them in position when bed turning * hatches to lift up when assessing for pressure ulcers or cleaning or dressing care --> also can void through hatch computerized --> how fast and how decrease pulmonary complication --> alveolar to open up, reducing skin pressure ulcers, preventing bladder stasis *how often to do stop --> once a shift to assess--> but moves very slow so can do assessment NURSING DX -impaired mobility -motion sickness -coping -knowledge deficiency

TYPES OF STROKE

ischemic -thrombotic (most common (60%) -embolic --> symptoms more severe, occurs suddenly Hemorrhagic Stroke ---Arteriovenous Malformation (AVM) ---Aneurysm

MG --> DRUG THERAPY * corticosteroids --> dose, name * immunosuppresive therapy (3 names), used with what

Corticosteroids alternate day frequency→ one day 5 next day 15 → suppresses immune response Prednisone**most common 80% have marked improvement Immunosuppressive therapy azathioprine (Imuran) Mycophenolate (Cellcept) Cyclosporine (Sandimmune) used in conjunction with corticosteroids

cranial nerves 3 cranial nerves 4 and 6

Cranial 4 + 6 → gaze Cranial 3 → pupil rx

Postural hypotension (orthostatic hypotension)

D/T DECREASED VENOUS RETURN TO HEART UPON SITTING & STANDING CAUSED BY POOR MUSCULAR TONE (higher injury) ASSESS VITAL SIGNS PRIOR TO & DURING OOB ELEVATE HOB AT LEAST 10" PRIOR TO OOB***--> elevate head before this to see how they are doing keep checking pressure ABDOMINAL BINDER, TED STOCKINGS, ACE WRAPS--> trying to push blood right back to the heart May need anti-hypotensive drugs, ***Midodrine is a vasocontrictor * poor sympathetic tone * poor muscle tone (higher spinal cord injury)

LINEAR SKULL FRACTURE

DEBRIDE & IRRIGATE WOUND IF NEEDED→ may have glass, a lot of bleeding (want to stop) If they don't know how long wound is open or been open for a while will not close it all the way→ continue to do dressings → let it heal by secondary intention to prevent infection ASSESS FOR INFECTION Crack in skull → just let it heal for linear (potential for underlying injury though)

PE COMPLICATION -pulmonary infarction

DEF--> death of the lung tissue most likely when there is 1. occlusion of large pul. vessel 2. insufficinterm-138et collateral blood flow 3. preexisting lung disease leads to alveolar necrosis and hemorrhage usually with occlusion of a large PE poorer outcomes

Subdural Hematoma -def -type of bleed -categories

DEF: Blood between dura mater and arachnoid membrane Tearing of bridging veins between brain and dura→ due to tramatic injury OFTEN A VENOUS BLEED→ slower Categories: Acute: s/s in 24-48 hours Subacute: s/s 2 days to 14 days later Chronic: s/s after 2-3 weeks, even months

phlebitis -definition -MANIS -RISK FACTORS

DEF: inflammations of the superficial vein usually in arm / hand (acute inflammation) (small superficial veins) MANIS: warmth pain tenderness erythema→ quickly resolves after catherter is removed swelling RISK FACTORS usually associated with IV Catheter or Irritating drugs if medications that caused this → make sure go to formulary → if vesicant may have to do a few interventions

Sensory: How Do you Determine the Level? and motor

DERMATOMES--> muscle group that is innervated by particular cervical, thoracic or lumbar nerve -check areas side to side --> helps find out where lesion//sci is will do this hourly b/c edema and hemorrhage can change how the patient expresses sensory --> pin or light touch (cotton swab) need to be awake enough for them to respond--> if comatose wont know sensory -usually feet to head

VTE PREVENTION -assesment -prevention

DVT assessment Leg circumference Doppler ultrasound--> inacute and rehab Signs and symptoms (sensation or not) DVT prevention Encourage OOB, perform ROM Pneumatic Compression Boots (PCBs) or Ted stockings Lovenox SQ--> LMWH

DEPRESSED SKULL FRACTURE

Debride and irrigate Protective device; position away from defect If >5 MM depression → surgery; acrylic cranioplasty within 24 hours or 3-6 months later May just wear a protective device or put a acrylic cranioplasty→ THINK ABOUT MRI \Depressed skull FX→ ping pong ball → if hit it hard enough encapsys over it self

Posturing (decorticate vs decerebrate)

Decorticate - remember arms to CORE - reflects cereb. Cortex problem Decerebrate - poorer prognosis - lower cerebellum, brain stem problem Give example of differences between these manifestations - they get mixed up! Patient is posturing → means decerebrate/decorticate

IV THERAPY -what kind of solution

Decrease cerebral edema → HYPERTONIC SALINE solution in the vessels → this solution pulls the excess fluid from the tissue into the vessels and urinate it out → just for a couple days (3% sodium chloride bag)(don't want to over due the IV because dont want to do it so fast) -this can reduce swelling and promote blood flow in the brain -requires frequent monitoring of BP and sodium serum levels b/c intravascular fluid volume can occur

CASE STUDY...Initially, your patient's bowel sounds were absent but now they are +. He has progressed from TPN to a regular diet. He begins a bowel management program.See Table 60-10 in Lewis, et al., p. 1433 for Patient Teaching, Bowel Management

Decreased GI motor activity contributes to development of Paralytic ileus Gastric distention - Nasogastric tube If cord injury is above conus medullaris- do not sense full rectum - reflexive BM (incontinence) If cord injury below conus medullaris - areflexic bowel, stool propulsion is slow, sphincter relaxed (retention)

NURSING DX (3)

Decreased intracranial adaptive capacity related to decreased cerebral perfusion or IICP Risk for ineffective cerebral tissue perfusion related to reduction of venous and/or arterial blood flow and cerebral edema Risk for disuse syndrome related to altered LOC, immobility, and altered nutritional status

TYPES OF SKULL FRACTURES

Depression fracture Compound fracture → through the skin Hairline fracture (linear) Subdural hematoma

NON-Contrast Head CT (stroke diagnostci) -why used -determines what

Differentiate between ischemic vs hemorrhagic Determine size and location ischemic stroke → can take 6-8 hours to show up on a cat scan SO WITH CAT SCAN we are looking to see if it is a bleed → we DO NOT WANT to give TPA with Hemorrhgaic stroke blood shows up as white determine the size and location

Pateints with right side stroke

Difficulty in judging position, distance, and movement Impulsive, impatient, and deny problems related to stroke Respond best to directions given verbally

s/s of concussion -cognitive

Difficulty thinking clearly Feeling Slowed down Difficulty concentrating Difficulty remembering new info Retrograde amnesia→ right before the event

DRUG THERAPY FOR ICHEMIC STROKE -name when given -how given -monitor what -when is it not given -what test is performed

Do not delay fibrinolytic therapy Tissue plasminogen activator (tPA)--> helps lyse the clot give IV → in order to administer quickly, establish blood flow through blocked artery Monitor VS and neuro status - don't give if improving Remember BP control Administer within 3-4.5 hours of S/S→ even if 5 hours out of that window Screening: CT scan, coag studies Hemorrhagic stroke - not given!******* GI bleed, head trauma/stroke within the past 3 mos. Major surgery within past 2 wks. INR > 1.7 No anticoagulants/antiplatelet drugs for 24 hrs-48 hours Anticoagulants after patient has stabilized May then go for neurointerventional procedure

ACUTE CARE FOR HEMORRHAGIC STROKE -drug theraoy - for what -prophylaxis for what

Drug therapy Management of hypertension**** Oral/IV agents Which drugs are best? to manage BP IV LIBETOL, ORAL → maybe transition Seizure prophylaxis → blood is very irritating need side rails and suction at bedside Reversal agents for anticoagulants→ in the other lecture know Manage ICP

COMPLICATIONS: Respiratory Depression * how much time * what can cause * what level of spine * nursing dx * number one killer? *chest pt

During first 48 hours, spinal cord edema increases level of dysfunction. Respiratory distress may occur. Injury at or above C3 Patient is exhausted. Labored breathing/ABGs deteriorate. Endotracheal intubation/tracheostomy (if know pt is c2 injury and rehab--> may trach them right away and vent them) Mechanical ventilation NURSING DX ineffective airway clearance, breathing patterns, gas exchange NUMBER ONE KILLER : pneumonia Respiratory arrest a possibility Other potential problems Pneumonia and atelectasis--> listening to breath sounds, lung expansion, respiratory rate Nasal stuffiness and bronchospasms Aggressive chest physiotherapy--> can also teach them to do it home done after the stabilization of the spinal cord (and should have an order) Adequate oxygenation Proper pain management

CASE STUDY...Your patient rings his call bell. He complains of a terrible headache. He is extremely sweaty and his face looks flushed.

Dysreflexia

SUPERFICIAL VEIN THROMBOSIS -etiology -manis -risk factors

Etiology Formation of a thrombus in a superficial vein Greater or lesser saphenous vein *** → these are superficial Manifestations: Palpable, firm subcutaneous cordlike vein Area surrounding vein-tender, reddened, warm Extremity edema may or may not be present Risk factors: Age, pregnancy, obesity, after treatment for varicose veins (sclerotherapy), recent surgery, long distanced travel, history of venous insufficiency

RISK FACTORS --> ALS

Genetic → 5-10% Veteran's → chemical exposure More common in white males

MANAGEMENT OF AD -actions -meds

ELEVATE HOB STAT!--> drop pressure until get more help, fastest way to treat FREQUENT VS--> autonomic bp cuff TREAT POSSIBLE CAUSES --> check cath, when last time bowel movement, are they in pain, did we just turn them MEDS: ATROPINE--> this is for bradycardia, may also increase Bp NTP, PROCARDIA, NIPRIDE, HYPERSTAT PREMEDICATE FOR PROCEDURES MEDI-ALERT BRACELET PATIENT TEACHING - Lewis, et al., Table 60-7, p.1431

GBS --> etiology * most common

EXACT cause is unknown Viral or Baterial infection cytomegalovirus and Campylobacterijejuni → most common gastroenteritis

ACUTE CARE -elimination deficits

Elimination deficits Often temporary If stroke only affects one side: Partial sensation for bladder filling intact, voluntary urination present May experience frequency, urgency, incontinence initially--> can be improved with retraining techniques Constipation associated with immobility, weak abdominal muscles, dehydration, diminished response to defecation reflex

INITIAL CARE

Ensure patent airway. Stabilize cervical spine. Administer oxygen via nasal cannula or non-rebreather mask. Establish IV access with two large-bore catheters to infuse normal saline or lactated Ringer's solution as appropriate. Assess for other injuries.***--> pneumo, hemo, fractures Control external bleeding. Obtain imaging.--> CAT SCAN and check brain at same time --> usually not with dye because takes too long Prepare for stabilization with tongs and traction.-->. cannot hold head forever

OTHER DRUGS Catechol O-Methyltransferase (COMT) inhibitors:

Entacapone and tolcapone block the enzyme that breaks down levodopa in the peripheral circulation, prolonging the effects of Sinemet.

Blood Pressure Management -dont wnat to drop why * recommendations by AHA

Evidence based practice national guidelines recommend acute Ischemic stroke patients should not have their blood pressure lowered too quickly (first 72 hours).--> BECAUSE IT DECREASES CEREBRAL PERFUSION --> want to keep it at a certain number AHA/ASA Recommendations for BP treatment: *Ischemic stroke: Treat BP if > 220/120 *TPA patients keep < 180/105 24hrs post TPA--> do not like it too high when TPA -need to have parameters on how to titrate meds American Heart Association and American Stroke Association advise against the use of tPA when systolic BP reaches above 185 mm Hg.

what type of person is prone to chronic SDH

Examples of chronic causes- shaken baby syndrome, homeless person who is prone to falls but no one sees them, danger of those who are on anticoags and have falls or are in MVC someone who keeps hitting their head and don't realize they have the injury → EX is a boxer → initially the s/s will not be there if blood leak was small another example is → coumadin, fall alot , drug addict, if alone and fall you may forget you fell, changes in LOC

SPASTICITY -def -heightened when -aggravated by what

Excessive muscular tone & exaggerated DTRs of antigravity muscles (arm flexors, leg extensors) heightens 1-2 yrs after injury aggravated by cold, anxiety, stress, fatigue, impaction, decubiti lifetime challenge * altered comfort * impaired mobility

FAST --acronym

FAST → time is crucial medical emergency need to get help to decrease death and disabilies FACE → does the face look uneven, have them smile ARM→ does on arm drift down when hold them up (ask them to raise both arms SPEECH→ does their speech sound strange (ask them to repeat a phrase) TIME → every second brain cells die and more complications , call 911 right away for any signs of stroke

Flaccid -what neurons

FLACCID LOWER MOTOR NEURONS NOT FUNCTIONING INITIALLY SEEN IN SPINAL SHOCK

Priority Interventions : Electrolyte Balance

Fluid & electrolyte balance Hydrate 1500-2000 ml/day Watch for alteration in ADH secretion→ messes up when brain become irritated NSS for IV solutions preferred

Skeletal Traction -nursing assessment -what should the nose align to -nursing dx

For injury reduction/re-alignment WEIGHTS FREE-HANGING--> should not be resting on floor PIN SITE ASSESSMENT & CARE--> right in the skull, may be cleaning them sterile saline q 4 hrs, or with peroxide --> depedning on institution --> may also have brain sponges --> risk for infection SUPPORT HEAD WHEN POSITIONING IN BED--> when turning them --> now they have traction (remember someone always in charge 1,2,3 and turn) ALWAYS ALIGN HEAD WITH BODY NOSE SHOULD ALIGN WITH UMBILICUS AFTER POSITIONING--> so the spine is in alignment IMMOBILITY RISKS Nursing diagnosis -altered skin integrity -risk for infection -impaired mobility -skin integrity --> pressure ulcers -acute pain (at lesion and below) -coping

Nursing Planning and goals

Goals: the patient will Maintain stable or improved level of consciousness Attain maximum physical functioning Maximize self-care abilities and skills Maintain stable body functions Maximize communication abilities Avoid complications of stroke Maintain effective personal and family coping

What is the defining factor of whether it is ischemic or hemorrhagic ???

HEADACHE → hemorrhagic stroke

COMPLICATION: VASOVAGAL RESPONSE * how to prevent * triggers * tx what to have at bedside and med

HYPEROXYGENATE PRIOR TO SUCTIONING--> helps to prevent this SLOW POSITION CHANGES--> they may hold breathe -can also occur during bowel movement, gagging ATROPINE IF SYMPTOMATIC--> on bed side table BRADYCARDIA OCCURS TEMPORARY/PERMANENT PACEMAKER *high injury

pronator drift test

Have pt stretch out arms with palms facing up and close eyes. Positive if one arm goes downward or drifts.

Positoning of the patient -purpose

Head of bed elevated 30 Promotes jugular venous drainage ** PURPOSE → veins draining this excess fluid Head in alignment with body when positioning

Myasthenia Gravis --> Diagnostics

History and physical electromyography (EMG) assesses the health of muscles and nerve cells that control them (motor neurons→ transit electrical signals that allow for contraction Tensilon test (edrophonium chloride) It is an anticholinesterase agent that blocks the enzyme acetylcholinesterase→ the enzyme that breaks down Ach. Briefly improves muscle contractility (+ results) Also used to check for cholinergic crisis (too much anticholinesterase drug)** need to be careful MRI/ CT looking at the thymus gland

Interprofessional Care--> nutritional therapy -what state are they in (2) -what kind of feedings may they be on -what state -IV fluids???

Hypermetabolic and hypercatabolic state ↑ need for glucose parenteral nutrition→ if not bowel sounds Enteral Early feeding (within 3 days of injury)--> better outcomes Keep patient normovolemic.(may be a little dehydrated def not overloaded tho) IV 0.9% NaCl preferred over D5W or 0.45% NaCl--> we do not want this b/c serum osmolarity will decrease and cerebral edema may increase

examples of CPP

ICP 15 BP 130/80 MAP 96 CPP: ___ ICP 30 BP 130/80 MAP 96 CPP: ___ Bp did not change ICP 30 BP 150/80 MAP 108 CPP: ___ Bp also goes up→ shows you that it is better CPP→ shows they may need bp up to maintain CPP This is also the widening pulse pressure → to maintain CPP So, increased SBP, widened pulse pressure to maintain CPP. CPP VALUES : 60-100 normal CPP Less than 50 CPP neuron death; less than 30 ischemia

what is the treatment of neurogenic shock -think low bp and low hr

IV FLUIDS--. increase Vasoconstrictor drugs (ex--> epinephrine) Atropine no blood transfusion or BETA BLOCKERS--> b/c low bp and hr

VTE : SURGICAL INTERVENTIONS -vena cava interruption devices

IVC filter (inferior vena cava filter) filter put into inferior vena cava and traps that blood clot so that it doesn't travel up and hit those more central areas The only widely accepted and validated indications for vena cava filter placement are an absolute contraindications to therapuetic anticoagulation, complication to anticoagulation and failure to coagulation when there is acute proximal venous thrombosis

Immunoglobin G

IVIG→ defense proteins to help improve immune function→ not sure the mechanism of action just know defense and sometimes works and sometimes doesn't

OCULOVESTICULAR RESPONSE

Icy cold water to ear , HOB @ 30 degrees, 5cc in ear canal → eyes should deviate towards the ice water and then away NORMAL→ eyes deviate to side of ice water application ABNORMAL→ eyes do not deviate → could be brain dead

Interprofessional Care for VTE (4)

Identify high risk patients Early mobilization Compression stockings Pneumatic compression devices

PRE SWALLOWING SCREEN -know the nurse can do this

If "no" is a response to any of the questions below, discontinue swallow screen and obtain an order for a speech and swallowing evaluation. Is patient awake/alert? yes, continue / no, stop, NPO Can patient sit upright? yes, continue / no, stop, NPO Can patient cough? yes, continue / no, stop, NPO Can patient control saliva? yes, continue / no, stop, NPO Can patient lick both lips? yes, continue/ no, stop, NPO Can patient breathe freely? yes, continue / no, stop, NPO Does patient have a clear voice? yes, continue / no, stop, NPO (ANYTHING NO --> THEY GO NPO) If "yes" is a response to any of the questions below, obtain an order for a speech and swallowing evaluation. 1st tsp water with spoon: no symptoms, continue / yes symptoms, stop, NPO 2nd tsp water with spoon: no symptoms, continue /yes symptoms, stop, NPO 3rd tsp water with spoon: no symptoms, continue / yes symptoms, stop, NPO 3oz/90mL water with cup: no symptoms, continue / yes symptoms, stop, NPO Symptoms that indicate failure can include choking, coughing, throat clearing, gurgly sounds, or leakage from the patient's mouth. Speech and Swallowing Consult order obtained? yes / no

Nursing interventions -controlled hyperventilation -what state will they be in and why is this good SHORT term*

If on ventilator hyperventilate them get respiratory alkalosis → why is this good → constricts arterioles and decreases the cerebral blood volume in the brain Blow off pCO2 Constricts arterioles, decreases cerebral blood volume ***--> skull is prison for brain // it cannot expand -_> if we can constrict these vessels → more room for the edema REMEMBER RESEARCH!!! Used to really hyperventilate them for a whole week → HOWEVER now we are making this person ischemic and not perfusing the brain Caution → severe hypocapnia may cause ischemia

NEURO CHECKS

If patients are very agitated, intensely seizing or have frequent posturing (decerebrate/decorticate), may sedate them. Talk about the influence of care and family visitation - may need to space out activities - some families can actually increase ICP while others are calming and can decrease ICP. Need to individualize care. Sometimes docs will tell you to hold off until you do a neuro check → some of these meds can mask what is really going on

PD --> NURSING DIAGNOSIS (5)

Impaired physical mobility related to rigidity, bradykinesia and akinesia Impaired verbal communication related to dysarthria, tremor, and bradykinesia Imbalanced nutrition: less than body requirements related to inability to ingest food Impaired swallowing related to neuromuscular impairments (gag reflex issues) Risk for decreased self esteem due to impaired cognition, tremors, and self-care deficit

WHAT IS THE COMMON THREAD RELATED TO MANIFESTATIONS AND TREATMENT THAT LINKS THESE FRACTURES?

Increased ICP, cerebral edema and bleeds → this is how you treat them

suregery -indications types

Indications: if neuro deficit progressing; if compound fracture or penetrating wound(getting worse, fractures etc) ORIF with wiring of cervical spine & fusion Decompression laminectomy-_> remove the mania that is out of line Rodding may decrease spinal cord injury

*WHAT CONCERNS DO YOU HAVE RELATED TO THE PATIENT'S LEVEL OF INJURY AND HIS RESPIRATORY STATUS? -where on the cord

Injury at or above C4: phrenic nerve paralysis → won't be able to breathe Can/will respiratory arrest Need mechanical ventilation Track vital capacity (max exhale after max inhale) - 15-20 ml/kg is normal -level of the injury --> has effect on how much support they need Below level of C4*** Diaphragmatic breathing if phrenic nerve is functioning Spinal cord edema and hemorrhage can affect function of phrenic nerve and cause respiratory insufficiency.--> SECONDARY INJURY Hypoventilation almost always occurs with diaphragmatic breathing.--> abgs--> hypoventilation will give resp. acidosis

s/s of concussion -emotional

Instability Sadness More emotional Nervousness anxiety

ACUTE C ARE -integrumentary * what are factors that may increase risk * how do we prevent skin breakdown

Integumentary Susceptible to breakdown Compounding factors may increase the risk--> age poor nutrition, edema and incontinence How can we prevent skin breakdown? Pressure relief-CHANGE positions Skin care Early mobility Skin barriers--> barrier creams metalex

CONCUSSION

Know discharge instructions → tabel 56-11*** Rest, no computer, tx , take time off from class → want to make sure brain and neurons recover and do not want to overuse Often they are not admitted to the hospital but need to be tracked When would they return to the hospital??--> Repeated concussion can lead to long-term debilitating conditions such as chronic traumatic encephalopathy → a progressive degenerative disease ) and post concussion syndrome → why so important to follow discharge instructions Look for ha getting worse or changes in personality -things are getting worse, ha, need someone home with them, only ct scan if lost conciousness -no computer, tv, screens

autonomic dysreflexia -where affected what haooens -s/s -common triggers of dysrflexia

LESIONS at T6 and above NOXIOUS STIMULI CREATES EXAGGERATED SYMPATHETIC RESPONSE BELOW LESION - VASOCONSTRICTION REFLEX BRADYCARDIA & VASODILATION ABOVE LESION - DUE TO BARORECEPTOR STIMULATION S/S: INCREASED BP*** PILOERECTION BELOW LESION PALLOR BELOW LESION BRADYCARDIA HEADACHE DIAPHORESIS & FLUSHING ABOVE LESION*** COMMON TRIGGERS OF DYSREFLEXIA DISTENDED BLADDER DISTENDED BOWEL SKIN BREAKDOWN OR PRESSURE// skin pinched URINARY TRACT INFECTION LABOR--> SCI can have children but need to know its s possibility think about the causes if they have these symptoms

LOGROLLING

LIFT & TURN PATIENT AS UNIT - A "TEAM" TURN!!! CONSTANTLY SUPPORT HEAD--> someone at the head is the cheif SUPPORT LENGTH OF SPINE WITH BLANKETS/PILLOWS--> to stay in alignement even when turned -when putting on backboard -keep spinal cord in alignment * 1 2 3 turn --> everyone at the same time --> slide board under (inspect back) we wnat no further injury

epidural hematoma -location -interruption of what artery -what kind of bleed means what -classic s/s

LOCATION: Between dura and inner skull surface Interruption of middle meningeal artery notice this is an artery → means it is a faster bleed Classic S/S: loss of consciousness, awake, then coma ex) fine talking to coach and when leave to the hositpial coma interruption of neurons → causes the quick lost of consciousness 55% have these classic other will just have some ICP changes ARTERIAL BLEED = FASTER PROGRESSION

stroke diagnostic test continued -labs and other tests

Labs Coagulation factors→ look at pt and INR → would not give TPA if INR is above a 7 CBC Electrolyte panel→ looking for abnormalities Blood glucose → b/c hypoglycemia can mimic stroke like symptoms cannot move their extremities be confused slurred speech etc→ can mimic what a stroke looks like Lipid profile Cardiac markers→ rule out any other problems → do troponin CXR→ chest x-ray EKG→ to see if they are having afib or flutter to make sure we aren't missing anything Echocardiogram→ if there is an obvious clot that is the cause

PD --> patho -lack of what and where and explain // disrupts what balance -when are symptoms seen

Lack of dopamine in brain Pathologic process involves degeneration of dopamine-producing neurons in substantia nigra of the midbrain. Disrupts dopamine-acetylcholine balance in basal ganglia don't know what causes dopamine to become destroyed → needed for cns symptoms are not seen until 80% of neuron function is lost substanstia nigra

Summary of major S/S of IICP -late

Late: fixed pupils,(flashlight in eyes and no pupil response// blown pupils) extreme motor changes(decerabate/decorticate) or no response, loss of reflexes, VS changes (Cushing's triad) -cushing triad → can accumulate overtime → need to look at the bigger picture if keep decreasing HR or widen pp keep looking

COMPLICATION OF ICP ***HERNIATION -def -what vital signs -ICP may go into normal rnage why -what indicates an impending hernation

Leave normal anatomical position I don't have them memorize the types of herniation - rather generally what happens and then how they may manifest - ultimately Cushing's triad Note that once patient herniates, their ICP may go into normal range - look at whole picture - they may be at the point that they will not recover if brain death has occurred Deteriorating neuro signs but also CUSHING SYMPTOMS Widening pulse pressure, systolic rising, bradycardia, irregular respirations Once actually herniates → ICP may actually drop to normal → may seem good but have signs of brain detah ****VENTRICULAR SHIFT → IMPENDING HERNIATION → this is not a good sign → cat scan right away

NEUROGENIC SHOCK * def * what is it caracterized by?? nursing dx

Loss of vasomotor tone caused by injury Characterized by hypotension and bradycardia (important clinical cues) Loss of sympathetic nervous system innervation causes Peripheral vasodilation Venous pooling ↓ cardiac output cannot vasoconstrict nursing dx -decrease co, altered tissue perfusion

VTE (DVT) -manis

MANIS unilateral leg edema → only clot in right leg only in right pain tenderness paresthesia warm skin erythema febrile (greater than 38 degrees C) Homan's Sign -(not specific or reliable) - less than 10% present -hold hand under knee and flex and forsiflex foot up → if feel pain may be a sign

GBS --> MANIS * what kind of paralysis // begins where and peaks when * first * max weakness is reached when

MANISFESTATIONS ascending symmetrical paralysis usually symmetrical weakness that begins in lower extremities (LE) and progresses over hours/days peaks around the 14th day Acute, rapidly progressing First symptoms weakness parathesia → numbness and tingling LE hypotonia → reduced muscle tone Weak or Absent reflexes Maximal Weakness reached in 4 weeks

PE --> MANIS --> MASSIVE PE

MASSIVE PE : impending doom change in mental status Hypotension about 10% of pts will impase if massive PE

Leveling the VENTRIC

Make sure 0 on chamber matches 0 → foramen of Monroe CSF normally clear yellow → if bleed may be pink if infection may be cloudy

MS MANIS -sexual Dysfunction

Male: Erectile Dysfunction Female decrease libido, difficulty with orgasm, painful intercourse, decreased vaginal lubrication Diminished Sensation

Monitor ICP -more common in what kind of stroke -peak ____ hours -positioning -control what

More common with hemorrhagic stroke**** Peaks in 72 HOURS Elevate head of bed → 30 degrees or more Keep head/neck aligned Control hypermetabolic states Hyperglycemia Fever Seizures: intracerebral and SAH

MG NURSING IMPLEMENTATION

Medication purpose, dose, side effects→ many interactions--> no OTC w/o permission No OTC meds without MD permission Medic-Alert bracelet Dietary precautions (chewing/swallowing difficulty)--> make sure on right diet Rest and activity→ if get fatigued may exacerabate their symptoms Perform physically demanding activities in morning Plan ADLs to avoid fatigue Complications of disease Myasthenic/Cholinergic Crisis Refer to the MG Foundation or MG support group goals of care, return to muscle strength, manage fatigue, avoid complication, maintain quality of life

Corticosteroids -used to treat what kind of attack // helps reduce what -does not change what -2 types

Methylprednisolone (IV)--> for more severe/acute attack Prednisone (PO) → for weaning or for chronic Helpful in treating acute exacerbations by reducing edema and acute inflammation at the site of demyelination*** Does not change disease progression

Summary of major S/S of IICP -moderate

Moderate: LOC changes, motor changes (contralateral to the injury), pupil changes (ipsilateral//same side), disconjugate eye movement(3/4/6), vomiting, headache, papilledema(optic disc edema)

PRIORITY INTERVENTIONS -VS --> most important -drugs

Monitor VS, particularly BP IV medications preferred in acute stroke Labetalol→ Beta blocker Nicardipine (Cardene)--> calcium channel blocker elevated→ this can be seen → this is a protective measure to help cerebral perfusion → however we do not want it too high therefore give these too medications

Surgical options --> most common and what it is

Most common is deep brain simulation** Places an electrode in the thalamus, globus pallidus or subthalmaic nucleus (under clavicle) Utilizes a generator to deliver specific current to the targeted brain location safer and more programmable than ablation shown to improve motor function, reduce dyskinesia and medication usage

Acute care of stroke -what is the most important thing -what are the goals

Most important is patient history and time of onset of symptoms Goals: Preserving life Preventing further brain damage Reducing disability (why time and money is so important)

CLINICAL MANIS -motor -which side

Motor Most obvious signs of a stroke--> can have paralysis or weakness that can--> Can cause impairment of: Mobility Respiratory Swallowing and speech Gag reflex Self-care abilities Remember because of pyramidal pathways crossing at the medulla a problem on the one side of the brain will affect motor function on the opposite side (contralateral)***** RIGHT SIDE STROKE --> SIGNS ON LEFT

OTHER DRUG THERAPIES * muscle relaxants --> help with what * CNS stimulants * anticholinergics *tricycleantidepressants *selective potassium channel blockers * Antisiezure drugs

Muscle relaxants→ to help with spacsity CNS stimulants (fatigue) RITALIN (ex) Anticholinergics (incontinence//bladder symptoms) Tricyclic antidepressants (for paresthesia) used for pain or parethesia Selective potassium channel blocker--> DALFAMPRIDINE (AMPRYA) (improve ambulation, fatigue, endurance) help improve nerve conduction in damage nerve areas be careful if they have a hx of seizure disorder or kidney disease Antiseizure drugs (paresthesia and optic neuritis) ex) why are they taking these weird meds if they have MS → b/c based upon the symptoms

ACUTE CARE -musculoskeletal

Musculoskeletal Maintain optimal function by prevent joint contractures and muscular atrophy ROM exercises and positioning Trochanter roll at hip to prevent external rotation Hand cones to prevent hand contractures--> look at pictures, may also see foot drop--> have difficulty lifting foot, may have a boot or splint Arm supports with slings and lap boards to prevent shoulder displacement Avoidance of pulling the patient by the arm to avoid shoulder displacement Posterior leg splints Hand splints to reduce spasticity

MS DIAGNOSTIC TESTS * is there a definitie tests * MRI --> looking for what * CSF --> Looking for what * evoked potential responses --> looking for what

NO definitive diagnostic test for MS Based primarily on history, clinical manis, and results of certain diagnostic tests MRI of brain and spinal cord → presence of plaques (very small plaques in brain and spinal), inflammation, atrophy, and tissue breakdown and destruction cerebral spinal fluid (CSF) analysis → INCREASE immunoglobin G, presence of oligoclonal banding Evoked potential responses → often delayed because of decreased nerve conduction form eye and ear to brain→ tests sight sound touch

Sensory - Perceptual -neglect -homonymous hemianopsia

Neglect Uni-lateral Left-sided neglect→ completely leave the clock off → dont recognize it is there → very important when assess pateint do not want to approach them on that side https://www.youtube.com/watch?v=35ggDdoRAKo Homonymous hemianopsia→ blindless in same half of each visual field → important when setting up their food make sure in visual fiels

CONTINUOUS EEG MONITORING AND BIS

Neuro ICU nurses may be trained to read simple EEG waves but neurologist/neuro NP are usually responsible

sexual counseling

No birth control pills or IUDs Diaphragms, condoms, spermicides recommended May have decreased sexual satisfaction, decreased sexual activity Use alternate ways to achieve sexual satisfaction

ALS --> COLLABORATIVE MANAGMENT -tx? -drugs (2)

No cure and treatment options limited Riluzole (Rilutek) Oral medication Slows the progression of ALS Reduces damage to motor neurons by decreasing the release of glutamate in the brain ***glutamate is excitatory neurotransmitter Edaravone (Radicava) IV daily for 14 days then no meds for 14 days Lessen the effects of oxidative stress--> oxidative stress process is a factor in role of ALS

other vasopressors for shock

Norepinephrine (levophed) orPhenlyEphrine (Neosynephrine) -continuous drug drips give them on parameters by NP or Physcian -make sure know half life when going up and down on drug drip

CVI -Patient education

Patient Education worn daily, replaced every 4-6 months, application is important → correctly put on Activity avoid standing or sitting for prolonged periods of time sitting decreases that blood return from the lower extremities elevate legs above the level of the heart encourage walking -nutritional therapy

MANNITOL -normal serum osmo levels -mannitol osmo levels -goal of tx -check what before giving -give q ___ hours

Normal serum osmo is 260-300; goal of Mannitol is to get the to higher normal or a little bit high - for example 305-315 may be the goal Often orders are q 6 hours - check serum osmo before giving - there will be "hold orders" from MD/NP if too high (can dehydrate patient)***** Slightly dehydrated but not too dehydrated Goals serum osmo 305-315→ want it a little higher to drain out that edema Think about the GOAL → DECREASE ICP → look for this outcome I usually ask them how would you know the Mannitol work? - they usually give me the actions of the drug - but the goal is to decrease ICP - that is what we want as the outcome

Halo - VEST * def * inspect what * nurisng dx

Note the rigid shoulder straps and encompassing vest. Various vest sizes are available prefabricated. The halo ring, superstructure, and vest are MRI compatible. **ALWAYS INSPECT THE SKIN-_> for pressure ulcers, change the fleece risk for infection, skin integrity the pt may be able to walk if have function of legs SHIRTS or fleece under vest

ACUTE CARE -nutrition

Nutrition Nutrition needs to be addressed within 24 hours IV infusion initially to maintain fluid and electrolyte balance Dysphagia is common Need to have a swallowing evaluation complete Screening can be completed by nurses May need enteral or parenteral support--> if they dont pass swallowing screen

NURSING IMPLEMENTATION -nutritional considerations -bladder control

Nutrition Considerations minimize caffiene intake nutritious well-balanced meals increase roughage if constipated high fiber → helps with constipation Bladder Contorl medication adherence (anticholinergics) self-catheterization** Nursing Diagnosis, Urinary retention Treatment Regimen management of medication know drug se, interactions, otc and perscriptive any non-perscriptive drugs need to notify HCP emotional adjustment

BEST MOTOR RESPONSE

Obeys commands→ 6→ squeeze hands and release Localizes pain→ 5 → maybe not awake and don't follow commands but will cough when suctioning or push away hand → know pain and pressure → purposeful movement but not completely conscious Flexion - withdrawal→ 4→ nail bed pressure and pull away → just a spinal reflex→ only push away Flexion - abnormal→ 3→ DECORTICATE Extension → 2→ DECEREBRATE No response→ 1 Untestable→ U

Major difference in the MANIS from Ischemic vs Hemorrhagic stroke

One of the biggest difference in sign and symptom is the sudden onset of a severe headache "thunder-clap"--> sudden onset of a severe HA, worst headache in my life

INterventions for sexual dysfunction

Open discussion with use of scientific terms Sexual counseling by expert Meds - Sildenafil (Viagra), penile injections Vacuum Devices with Constriction band Penile implant Consideration of bowel and bladder habits and preparation

EYES

Open spontaneously→ 4 To verbal command/name 3 → as soon as see name they open up To pain → 2 → nailbed pressure → pen in nail bed → this will move them → or also sternum rubs No response→ 1 → pain and nothing happens Untestable→ U want to record highest you see→ if you walk in and notice

Dabigatam (Pradaxa) * how given * use *antidote *onset

Oral (direct thrombin inhibitor) USE: VTE preventionafter elective joint placement, for stroke prevention for afib or tx option for VTE Antidote: Idarucizumab (Praxbind) Rapid Onset: do not need to monitor labs, lower risk for major bleeding all hematology recommendations → depending on underlying disease process

BEST VERBAL RESPONSE

Oriented & converses→ 5 Orienting x3 Disoriented & converses → 4→ person place time → one of these is not right Inappropriate words→ 3→ ex→ looking at a hat and calling it an orange Incomprehensible sounds→ 2 (groaning/talking under breathe just sounds) No response1

DRUG THERAPY --> VITAMIN K ANTAGONIST * pt education

Patient Education? no NSAIDs--> increase bleeding risk many drugs interactions and interfere with the bioavailability and mechanisms AVOID leafy greens → contain vitamin K and reverse the effects any procedures being done need to let them know on medications high risk for bleeding → watch razors, accidents etc, -also administer same time q day -may be affected by variation in some genes

SENSORY - PERCEPTUAL --> * other visual problems *

Other vision problems Diplopia - eye patch Loss of corneal reflex - protect against corneal abrasions with drops, ointments, eye shield at night Nursing Care of patients with visual field cuts & neglect Arrange the environment within patients' perceptual field, e.g. food, bedroom furniture, call bell, tv Patient learns to scan items on neglected side by physically turning self--> whole bosy Mark end of lines on book pages with line so they know when to stop or start

GBS --> PATHO

PATHO edema and inflammation of affected nerves loss of myelin sheath transmission of nerve impulses is stopped or slowed

Barbituate Coma -what drug -what does it do -need what -drug holidays why

PENTOBARBITAL→ IV drip OR loading dose then IVP q 6 hours Depresses CNS, CV, and RESPIRATORY SYSTEMS → alters assessment Need mechanical Ventilation and Total physical care Turn them mouth care skin care May assess effectiveness with continuous EEG (brain waves) or BIS Drug "HOLIDAYS"--> - take patient OFF med until pentobarb level closer to 0 so can do thorough neuro check**** And then put them back in Inform Family of Effects → tell them why they are on it (control ICP ) Don't give any false hope Use this if other forms of treatment have not worked

HAlo device nursing care -assess what -how do you clean -do not move the pt by holding what

PIN SITE ASSESSMENT & CARE - tightening by MD prn REMOVE PLATES/ vests TO ASSESS & CLEAN SKIN - no soaps, lotions, powders -one side of the time DO NOT MOVE PATIENT BY HOLDING ONTO HARDWARE WRENCH (a) or Allen Key (b) --> can help you undo the vest AT BEDSIDE - CPR--> incase they need CPR PSYCHOLOGICAL CONCERNS PATIENT EDUCATION--> need to know that if they are paralyzed not going to be able to walk // need to know why they have it (*********8Lewis et al., Table 60-6, p. 1428********* go over this -cannot drive -straw to drink -can get ha form the pins in the head -pain from chewing (tyelnol) -turn whole body when turning side ways not just the head and the neck -if vest becomes damp blowdryer -if emergency --> keep wrenches near pt at all times -mark vest strap to maintain consistancy and fit Nursing dx -knowledge deficieny -impaired mobility -risk for FAL:L**** --> very heavy

VTE DIAGNOSTIC STUDIES -lab work--> explain--> PTT, PT, INR, Hgb, Hct, Platelet count, and D-dimer

PTT, PT, INR→ looking at hypercoagulability Hgb, Hct→ are they anemic, do they have enough blood// are they losing blood Platelet count → are they clotting *D-Dimer* → fragment of fibrin formed from the fibrin degradation in clot lysis if elevated may be a type of formation and breakdown in fibrin clots in the body→ if elevated may need more imaging--> if elevated may signify a VTE imaging that may see is the non-invasous venous study or ultrasound it's not specific to DVT, PE, VTE → just shows that something is going on

T6 injury

Paraplegia, results in paralysis below the chest

STROKE ALERT -def -time s/s -if stroke is identified from this what do we call

Patient presents with suspected acute stroke by assessment of signs and symptoms and without known contraindication for t-PA: 3-4.5 hours from last seen well/onset of S & S s/s : weakness in arm, facial drooping, slurred speach get cat scan, neurologists, draw labs etc WATCH THE TIME!!!--> 3-4.5 hours if a stroke is identified we call a stroke code

COPING FOR STROKE

Patient's family should be given a careful, detailed explanation of what has happened to the patient Family members usually have not had time to prepare for the illness—social services referral is often helpful Plan family conferences - family response and adjustment to loss, possible guilt, anger, frustration --occurs suddenly and may not have time to plan for illness Manage atypical emotional responses with distraction, explanations to patient and family; avoidance of scolding and ridicule Encourage verbalization of feelings Discuss lifestyle and role changes Help identify person's strengths Establish achievable goals; encourage independence; provide praise Determine perception of and acceptance of body image

recommendation for assessment of ICP

Perform the neurological assessment with the nurse who just cared for the patient. This ensures complete understanding of the prior documented assessment by the receiving nurse and quick recognition of neurological changes.→ this makes sure not losing continuity of care and confirms you are seeing the same thing

Chronic Venous Insufficiency (CVI) MANIS

Persistent edema (can get so bad start leaking 4) increase pigmentation, leathery brown/brawny → from breakdown of RBCs--> hemosideron venous leg ulcers → painful -seen above the medial maleolus, pain, may have edema and infection--> pain may be worse when leg is in a dependent position Dermititis, Pruiritis** (very itchy) secondary varicosities

Peripheral Venous Disease : ACUTE (4)

Phlebitis Superficial Vein Thrombosis (SVT) Deep Vein Thrombosis (DVT) → encompanses the VTE Venous Thromboembolism (VTE)

OTHER MG TX plasmapheresis --> also seen in what, effective?, action IVIG--> action, benefits * these two tx are reserved for who and used for what

Plasmapheresis→ also with MS, filtering process similar to dialysis removes antibodies that block the transmission of symptoms effective but usually only last a few weeks, need the access to have this done IV immunoglobulin G→ normal antibodies which helps immune system benefits seen in less than a week and can last 3-6 weeks Reserved for people in crisis Short-term improvement in symptoms

IMPAIRED SWALLOWING & RISK FOR ASPIRATION -preparation for eating

Preparation for Eating Assess swallowing & gag reflex Elevate HOB 45-90 degrees if possible Create calm, non-rushed environment Select food easy to swallow with enough texture, temperature, and flavor--> help find favorite foods to encourage nutrition Removing unnecessary items from tray or table, reducing spills Perform mouth care prior to eating Consider assistive devices for eating--> pt and ot MAY POCKET THE FOOD ON THE SIDE AFFECTED --> have them open their mouth --> they have it in mouth

NURSING ASSESSMENT FOR STABLE PT

Primary assessment: History of current illness (symptoms, onset, duration, nature, changes in S/S) Past medical illnesses, particularly previous stroke, hypertension, atrial fibrillation Current medications→ if taking bp meds, anticoagulation, antiplatelets, statins for lipid control History of risk factors Family history of stroke Level of consciousness→ are they alert and oriented x4, alert, lethargic, stupor, comatose Cognition→ attention, perception, language Motor function→ compare both sides , should be plus 5 on both Cranial nerve function Sensation→ usually light touch Proprioception→ body's ability to sense location, movements and actions→ RHOMBERGS TEST → stand and close eyes and see if swaying Cerebellar function→ coordination, balance, posture DTRs→ deep tendon reflexes Stroke Scale (NIHSS)

ACUTE CARE FOR HEMORRHAGIC STROKES -some procedures done

Procedures may be done but depending where it is → (for intracerebral too deep may not be done)// subarcahnoid more possibility Evacuation of hematomas - craniotomy→ remove the blood and pressure on brian → take off part of skull and may remian open (and put in abdomen otherwise refridge) Clipping, wrapping, coiling of cerebral aneurysms Resection of arteriovenous malformations Ventriculostomy drainage of some bleeds→ seen in ICP lecture

Interprofessional care VTE -drug therapy -difference b/w prophylaxis and treatment of active -3 major classes

Prophylaxis anticoagulation prevents occurrence of DVT Treatment of active DVT prevents growth of DVT formation of new clots and embolization 3 major classes of anticoagulants Vitamin K antagonists Thrombin inhibitors Factor Xa inhibitors

PE SURGICAL THERAPY

Pulmonary Embolectomy (only severe situations and cannot receive thrombolytic therapy or did not work on these)--> need to be pretty unstable at this point because going to be on a heart/lung bypass machine -help decrease RV after load diagnostic imaging surgical approach Endovascular Invasive Procedures cath directed therapy eco's catheter one of name brands Inferior Vena Cava (IVC) filter--> used to prevent further emboli ---> inserted percutaneously in the femoral vein and placed at the level of the diaphragm in the inferior vena cava --> once inserted the filter expands and prevents migration of large clots in pul system

PE COMPLICATION Right heart strain

RV dilates due to overload blood comes from inferior vena cava → in RA → RV→ through pulmonary symptom→ right side of the heart is trying to pump but cannot pump because of the large clot and therefore more strain right ventricular dilation seen in acute

COMPLICATIONS -rebleeding * amount of time * what to monitor

Rebleeding First 24 hours highest risk Blood Pressure management vital pre-op SBP -goal→ determined by provider

craniectomy

Release IICP→ helps relieve the pressure → remove part of the cranium and allow the brain to come out to have lots of room Put bone in freezer or place in abdomen until brain edema subsides*** and then replace Care includes either wearing some type of helmet to protect that side and avoiding laying on that side

left arterial appendage occlusion

Removing or occluding the LAA decreases the incidence of strokes highly associated with stroke causing emboli esp. in AFIB

ACUTE CARE -respiratory --> PRIORITY

Respiratory Priority*** ABCS Increase risk for atelectasis and pneumonia--> Nursing interventions Frequent assessment of airway patency Oxygen therapy Suctioning Keep HOB elevated Cough and deep breathing Oral care

Degree of Injury Conus Medullaris Syndrome & Cauda Equina Syndrome *incomplete injury*

Result from damage to very lowest portion of spinal cord (conus) ***and lumbar and sacral nerve roots (cauda equina)*** Injury to these areas produces flaccid paralysis of lower limbs and areflexic (flaccid) bladder and bowel. sometimes called addle anesthesia checking for anal wink --> glove lubricate -- > and anus graps // winks finger --> to see if still functioning in this area

Nursing diagnosis for stroke

Risk for aspiration Impaired physical mobility Risk for injury--> coordination problems risk for falling and bleeding Impaired communication Difficulty coping--> devastating stroke Unilateral neglect

Intracerebral hematoma -s/s depend - > ____ml - what kind of bleed

S/S depend on location, size, & rate of blood accumulation > 5 ml. of blood blood is in the parenchyma depends on where the bleed is and where the blood accumlates → can be both an arterial or venous bleed 16% of TBIs -usually in frontal and temporal lobes

Levodopa-Carbidopa * SE * do give with what * what happens to the effect of drug // what do HCP do b/c of this * (3) other drusg

SE monitor for dyskinesia N/V Hypotension Do not give with food because protein reduces absorption Effectiveness of Sinemet could wear off after a few years of therapy therefore some initiate therapy with a DA receptor antagonist instead → Ropinirole (requip) or Pramipexole (Mirapex) or transdermal patch Rotigotine (neupro) In this case, Sinement is added when moderate to severe symptoms develop

MS MANIS -sensory

SENSORY blurred vision/double vision red-green color distortion blindness in one eye vertigo and tinnitus (ringing of ears) numbness and tingling Decrease hearing chronic and neuropathic pain→ PAIN MANAGEMENT is one priority

Spastic -what neurons

SPASTIC UPPER MOTOR NEURONS NOT FUNCTIONING FOLLOWS SPINAL SHOCK HELPS PREVENT PRESSURE AREAS BY PRESERVING MUSCLE TONE

Psychosocial Response

Shock, disbelief, denial Reaction- anger, depression Information seeking Coping/adjustment Nurse's role? Lewis et al., Table 60-12, P. 1435

S/S of Transient Attack -will they progress to stroke

Sign and symptoms depend on blood vessel and area of the brain that is ischemic Temporary loss of vision in one eye, hemiparesis, numbness, inability to speak, vertigo, ataxia, dysphagia, blurred vision 1/3 will not have any other TIA 1/3 will have other TIA 1/3 will progress to stroke

s/s of concussion sleep

Sleeping LESS/MORE than usual Trouble falling asleep

Patients with left side stroke

Slower in organization and performance of tasks Impaired spatial discrimination Have fearful, anxious response to stroke Respond well to nonverbal cues

What is the difference between spinal shock and neurogenic shock?

Spinal shock is mainly a loss of reflexes (flaccid paralysis) * usually with a high injury * mainly loss of reflexes, dtrs would not respond Neurogenic shock is mainly hypotension and bradycardia due to loss of sympathetic tone

GLASCOW COMA SCALE -def -3 categories -scoring

Standardized and concise assessment tool → convenient EYES BEST MOTOR RESPONSE BEST VERBAL RESPONSE TOTAL 3-15→ want closer to 15 8 or less → shows severe brain injury 9-12 = moderate injury < 8 severe injury "U" - UNTESTABLE

BASELINE LABS (5)

Stat Fingerstick blood glucose PT/INR, PTT→ coagulation factors CBC, Platelets Troponin, CK w/Isoenzymes Type & screen → blood type and screening +/-

CLINICAL MANIS

Stroke can affect many body systems Manifestations are related to artery involved Anterior cerebral→ motory and sensory deficiets Middle cerebral→ depending on dominant side → negelct motor sensory→ supplies blood to large portion Posterior cerebral→ visual motor disturbances Vertebral → visual, dysphagia, coma Manifestations depend on the side of the brain affected important to know where the injury is

Stroke core measures

Stroke education VTE Prophylaxis → PCP boots, Antithrombotic medication by day 2 Anticoagulation therapy for patients with atrial fibrillation Patients are assessed for rehabilitation TPA administered Discharged on antithrombotics Discharged on a statin medication

ALS--> nursing management

Support patient's cognitive and emotional functions by facilitating communication, e.g., "voice banking" allows a person to record a set list of phrases with their own voice, the recording is then converted to create a personal synthetic voice so when they are unable to speak they can use that synthetic voice Reduce risk of aspiration Early identification of respiratory insufficiency know respiratory assessment // what to look for Decrease risk of injury related to falls Decrease pain secondary to muscle weakness Provide diversional activities Assist family with advance care planning of disease process and anticipatory grieving their mind is sharp but their body is not do they want advance directives

Embolic Stroke

Symptoms more severe Occurs suddenly embolus forms in another part of the body and moves to the brain and blocks an artery -AFIB will probs be caused by a embolic stroke--> plaque breaking apart from endocardium and going into circulation (also MI, infective endocarditis, rheumatic heart disease, atrial septal defects, rheumatic heart disease) -manis --> occur suddenly and less collateral circulation ---pt usually remains consious with headache ---neurologic deficiet --> can be temporay if the clot breaks up -any age groups (ie--> rheumatic heart disease is a major cause in young to middle age adults) -warning signs are less common than thrombotic -recurrance is common unless underlying cause is prevented

Interprofessional care VTE -graduated compression stockings

TEDS need correct size → too small to constricted // too big not doing their purpose need skin assessments when you are giving bath -toe hole and heel patch in right place, nor wrinkles -if not worn properly venous return is impended and may increase the risk for: -arterial ischemia, edema , skin breakdown and VTE -enhanced if these stockings are used along with anticoagulation

PHLEBITIS -treatment

TREATMENT if phlebitis site associated with IV CANNULA → remove immediately elevation of extremity apply heat → normal saline or drug that is not a vesicant if it is a vesicant need to contact the pharmacy ot the formulary to see if there is a protocol (some do not recommend heat → varies drug to drug) mild oral analgesics(NSAIDS --> topical or oral)

Superficial Vein Thrombosis -treatment

TREATMENT oral NSIADs→ help with pain relief wear compression stockings → help with circulation warm compress→ try to decrease the edema elevation → decrease mild exercise → keep them moving What is the rationale?? ultrasound to confirm

TX OF BASILAR SKULL FRACTURE

TX BASILAR SKULL Minimize coughing, sneezing, valsalva maneuver → if dura teared CSF leak No nasal suctioning No nasogastric tube→ if hits tear nasogastric tube can go to brain area Do not pack nose/ears if CSF leak → COVER with sterile non-occlusive gauze Catch it so not dripping but don't want to pack it because bacteria can grow CSF → yellow (pinkish) if smelly or purulent --. Worried about meningitis Assess for infection → no support for prophylactic antibiotics *** NO RESEARCH Temp, wbcs, bands, fever, bad csf smell

C4 injury

Tetraplegia, results in complete paralysis below the neck -on ventilator

ACUTE EXACERBATION OF MS IS TRIGGERED BY WHAT(3)

UTIs URIs trauma

Assessment findings of stroke

These are found in both ischemic and hemorrhagic Hypertension--> will see if this is the major cause Facial drooping on affected side Difficulty swallowing Seizures--> esp. bleeding Bladder or bowel incontinence Nausea and vomiting Vertigo Altered level of consciousness Weakness, numbness, or paralysis Speech or visual disturbances Severe headache ↑ or ↓ heart rate→ depending how severe Respiratory distress→ esp. if they lose the ability to protect their airway Unequal pupils

Hemorrhagic stroke --> why complicated

These cause complications because blood is very irritating to this cerebral tissue and prevents it from getting the nutrients and O2→ irritation then causes the swelling to occur → further brian damage

CT angiography (stroke diagnostic)

Visualization of cerebral blood vessels→ and assess for blood flow in arteries using dye so need to look at kidney function and any other allergues May be done in conjunction with CT→ done with non-constrast

CORNEAL REFLEX

WHAT CRANIAL NERVE???--> trigeminal nerve → cotton in eye → BLINK If no blink brain death

changes in breathing pattern

This should be review from patho but just mention that resp changes can be a significant indication of IICP - especially when patients on ventilator, you notice the change in breathing pattern. CHENYE-STOKES → period of apnea, hyponia, there is a pattern but not normal CENTRAL NEUROGENIC → comes from brain stem -_> usually on the ventilator at this point→ respiratory ALKALOSIS APneustic → high apnea → big breathe in and out Ataxic → lower medulla, all over the place Hears patterns b/c hear ventilator → lower on the brain stem more irregular

MS PATHO -3 patho processes * what cells and what they disrupt

Three pathologic processes characterize MS Chronic inflammation Demyelination Gliosis in the CNS (proliferation of several different types of glial cells that often leads to scarring) Primary neuropathologic condition is an autoimmune process orchestrated by activated T Cells wbc attacks neurons and impact the fatty tissue near brain/spinal cord t cells are disrupting blood brain barrier → remember that activated T cells are WBCs→ very important to immune system and adaptive immunity → why it is called autoimmune process ---> subsequent antigen-antibody reaction within CNS activates the inflammatory response and leds to the demyelination Thymus → important in MS because where they mature

MG --> surgical options

Thymectomy Removal of the thymus gland→ they enhance the production of acetylcholine antibodies Indicated for those with thymoma→ tumor in thymus gland

Transient attack TX// ABCD SCORE

Treat as medical emergency→ whether or not they are admitted is based on the ABCDE→ score (age blood pressure clinical features, how long it lasts and pre-existing condition of dm) they will get a score Greater than 6→ 8% stroke within two days less than four 1% risk any score of 4 or greater would mean they need to be hospitalized

interprofessional care

Treat underlying cause. Adequate oxygenation PaO2 > 100 mm Hg PaCO2 35-45 mm Hg Intubation Mechanical ventilation → need to look at abgs and respiratory effort Surgery (craniectomy or craniotomy) May need a removal of the hematoma or the gunshot or the knife 25% glucose goes to brain

Drug therapy * how many drugs * excessive use of dopaminergic drugs lead to what * 3-5 years of tx pt experiences what and treated with --> taken with

Use of only one drug is preferred. Fewer side effects Dosages are easier to adjust. may be hard if the symptoms become worse → look at table in text (summarizes) Combination therapy is often required as disease progresses. Excessive dopaminergic drugs can lead to paradoxic intoxication. results in aggravation rather than relief of the symptoms Within 3 to 5 years of treatment, patients experience episodes of hypomobility "end of dose wearing off" or "spontaneous on/off". Treated with apomorphine (Apokyn) Needs to be taken with an antiemetic drug→ causes N/V--> not ZOFRAN THO

Diagnostic Studies of Stroke -at 10 min at 15 minutes within 25 minutes within 45 min 60 minutes??

Used to confirm stroke and likely cause of stroke Remember time of onset of symptoms imperative!!! → need to move rapidly Within 10 minutes to ED, HCP evaluates patient Within first 15 minutes in ED, stroke specialist alerted Within first 25 minutes, CT scan Within 45 minutes of CT, results interpreted MAX time for complete evaluation is 60 minutes!!!!--> needs to move fast

APNEA test

Used to determine brain death, as an indicator of central drive to breathe. Failure is no breathing after PaCo2 > 60 mmHg

Myasthenia GRavis --> MANIS

Usually a change in facial expression Speech may be slurred Muscles in trunk and limbs affected less Muscle atrophy is rare (not like ALS) No sensory loss// cognitve function intact Reflexes are normal Prognosis: Highly variable → some stabilize and others have progressive involvement

STeps of craniotomy

Usually behind the hairline → to hide scar A lot fo times shave head Not allowed to throw away hair → give the family a choice Use a vice to hold head still Open scalp w/ saw, use burr holes → to lift plate off, peel off derma, evacuate hematoma→ suction and release flap BURR HOLES: Sometimes burr holes are enough to evacuate a hematoma

etiology of Peripheral venous disease

VIRCHOW'S TRIAD→ leads to thrombosis formation

DRUG THERAPY --> VITAMIN K ANTAGONIST * other name * how take *action *how long does it take to become effective *ANntidote * what do you monitor and what is the range

Warfarin (Coumadin) taken PO, long-term action: inhibits activation of VK coagulation factors and anticoagulant proteins (c + s) * INR to monitor therapeutic levels q day typically based on provider orders around 2-3 but can vary b/w patient (normal INR is 1.1 or lower *takes 48-72 hours to become effective BUT several more days to be in maximum effect (typically parental anticoagulant is needed as well in first 5 days) *Antidote : Vitamin K (Kcentra)

common mechanism of injury

`All traumatic injuries include a description of the mechanism of injury Coup contrecoup can occur side to side too (car crash from the side for example) hit a wall in a car crash → injury at impact of concussion BUT ALSO a secondary impact → injury in front and back of the brain same thing if the head went from side to side bullet might be straight

TRUE or false → pupil size and reaction are considered part of glascow coma scale

→ FALSE → eyes on the glascow coma scale are more checking for

PHRENIC PACEMAKER

also known as diaphragm pacing, is the electrical stimulation of the phrenic nerve using a surgically implanted device. This device contracts the diaphragm rhythmically, improving breathing function in patients with respiratory insufficiency

ALS--> PATHO

brain messages fail to reach muscles muscles weakness and wasting results in denervation of the muscles and the lack of stimulation and use upper motor neurons and lower neurons exact cause is not known normal vs ALS als → a lot of wasting dendricytes are sagging, mtiochondrai dysfunction

Chronic Venous Insufficiency -def -patho

abnormalities of the venous system can lead to venous leg ulcers caused by leaking of serous fluid and RBCs from the capillary and venuoles in tissue damage to valves inside leg veins when bp does not drop when walking can lead to venous htn → can lead to ulcers forming → typically in ankle areas hemosideron --> brownish skin coloring from the breakdown of rbcs

NURSING DIAGNOSIS FOR VTE

acute pain blood clots are paininful impaired tissue integrity impaired physical mobility may not want to get up Risk for bleeding because of anticoagulation

Intraprofessional Care for VTE -what is it all about

all about prevention identify high-risk pts→ mandated by the joint commission need to identify these pts who is high risk?? immobile, surgery, new med (hypercoagulability)

mitoxantrone (Novantrone)-

antineoplastic - has serious side effect --> cardiotoxicity, leukemia, and infertility

Teriflunomide (Aubagio)

antinflammatory properties that reduce the amount of activated lymphocytes in the CNS * given orally -Treatment of relapsing forms of MS

Factors that influence ICP (8)

arterial pressure venous pressure intra-abdominal and intrathoracic pressure posture temperature decrease cerebral oxygenation hypercapnia (CO2 levels)

Complications of PD

as disease progresses, complications increase motor symptoms → spontaneous and involuntary movements weakness akinesia→ inability to move muscles freezing stooped posture masked face shuffling gait neurologic problems--> increase in mortality dementia neuropsychiatric problems depression, hallucinations, psychosis

MS PATHO -later stages

as inflammation continues in Ogliodendricytes → lose ability to regenerate the myeline --> loss of myelin sheath nerve damage loss of function (pernament) plaque formation→ from scar tissue white matter in CNS

Myasthenia Gravis --> PATHO * what gland

associated with tumors in the thymus gland → produce auto antibodies → and attack these acetylcholine antibodies and not allow the muscles to contract

MYASTHENIA GRAVIS * def * more commen in who * at what age men/women

autoimmune disease of the neuromuscular junction more common in WOMEN than in men onset in women before the age of 40 * onset in men after the age of 60

MS -ETIOLOGY * what kind of disorder * cause * theories of cause (4)

autoimmune disorder eact cause is unknown Some theories environmental influence lower vitamine D→ think that high latitudes less sun→ geographical variation Genetics increase chance if relatives Infection Epstein-Barr→ increase chances of MS Ethnicity most commonly hispanics, asians and africans

GBS --> manis ans dysfunction

autonomic Nervous System Dysfunction → mild to life threatening orthostatic hypotension hypertension abnormal vagal responses (bradycardia/Heart block) Bowel/Bladder dysfunction Pain, Paresthesia (worse at night) Variable sensory loss

PULMONARY EMBOLUS -def -where do they most arise from -where is the most common where they stop -what is a saddie pe

blockage of one or more pulmonary arteries where do most PEs arise from? the legs can be one or both sides (saddie PE) can be logged where the bification happens → more s/s -most common in the lower lobes of the lungs causes: are dislodged emboli but also air emboli (IV), fat emboli, bacterial emboli from the heart, amniotic fluid and tumors

MS --> NURSING IMPLEMENTATION * triggers * diagnostic phase * immobility

be aware of triggers -Infection (remember URI,UTI), trauma, childbirth, stress and changes in climate→ not everyone will have same triggers or response Reassure patient during diagnostic phase.--> even though it could be a tentative diagnosis need to also make sure they are aware of other neurological disease processes Assist patient in dealing with anxiety and grief caused by diagnosis.--> disabiliting illness Prevent major complications of immobility. → give them physical therapy, getting OOB--> avoid URI and UTI and pressure ulcer Focus teaching on building general resistance to illness. Avoid fatigue, extremes of hot and cold, exposure to infection Balance exercise and rest

Cerebral Circulation

blood is supplied to the brain by two major arteries internal carotid arteries (anterior circulation) vertebral arteries (posterior circulation) Both the anterior and Posterior circulation is connected to the CIRCLE OF WILLIS***** anterior and mid cerebral atery

CLICKER - How would you know if your patient had a deep venous thrombosis (DVT)? a. + Kernig's sign. --> sign of meningitis b. loss of peripheral pulses --> this ARTERIAL DISEASE c. warm, enlarged calf d. shortness of breath

c

PE --> MANIS

can vary and some are non-specific, can happen slowly or sudden (large) s/s will depend on size, type and extent of clot *dyspnea is most common* (85%)* may be hypoxic tachypnea cough, hemoptysis, fine** More common/course crackles fever tachycardia syncope

Cerebral aneurysm Coiling

cath inserted into the artery (via groin)--> neurovascular checks , monitor VS guide it to brain → tiny detachable coils to fill it → blocks blood flow into the aneurysma nd causes blood to clot blood wont go back in b/c no way can make back out

Incomplete spinal cord injury

central anterior brown-sequard Central: greater motor loss in upper extremities, variable sensory response; improves over time Anterior: complete motor loss, loss of pain sensation, loss of temp control below level of lesion; spares proprioception, vibratory sense, & touch Brown-Sequard: hemisection of cord; ipsilateral loss of motor, proprioception, vibratory sense, & touch; contralateral loss of pain & temp sensation

normal compenstaory mechanisms -ability to compensat??

change sin CSF Volume → can leave the brian and go down spinal cord → cause more pressure Changes in intracranial blood volume → can vasodilate or constrict Changes in tissue brain volume → brain tissue herniates→ leaves where it is supposed to be located Ability to compensate is limited if volume increase continues, ICP rises→ decompensation slow bleed but eventually will decompensate

Multiple Sclerosis -def// patho what happens -males or females -onset (most common onset) -avg life expectancy --> how they die -climate -ethic

chronic progressive degenerative disorder of the CNS Characterized by segmental demyelination of nerve fibers of the brain and spinal cord Females > Males females 2x more likely Onset: 20 to 50 years→ 30-35 most common avg life expectancy : >25 years don't die from multiple sclerosis but may from other factors such as immobility or completely unrelated cause climate --> more common in temp. climates of 45-65 degrees latitude (north us, canada, europe) (more than tropical) ethic--> less common in hispanics, asians and african descent -very rare in alaskan natives and aborgines

Hypercoagulability

cig smoking (increasing plasma fibrinogen and homocysteine levels) dehydrated sepsis (release of endotoxins) medications (corticosteroids and estrogens) imbalance of clotting mechanisms → leads to coagulation increase in fibrin products

TRAP

classic manis of PD tremors rigidity akinesia postural instability

ALS --> MANIS * most classic symptoms * how death

classic symptoms→ MUSCLE WEAKNESS Arms or legs may have cramping stiffness weakness in upper extremities (dropiuing things, tripping and abnormal fatigue of extremities, slurred speech, muscle cramps and twitches) MUSCLE ATROPHY larger muscles b/c lack of stimulation Dysarthria → slowed speech or difficult to understand dysphagia Muscle wasting and Fasciculations (twitching) Respiratory Failure (trach/ vent support needed) Death usually occurs from pulmonary infection, respiratory failure * does not change intelligence but may experience depression which can alter judgement and memory

PD --> impaired physical mobility

clothing adjustments → velcro, zippers, slip-on shoes elevated toilet seats remove rugs and excess furniture Consult physical therapy for personalized exercise program focus on strengthening and stretching include muscles used in speaking and swallowing

GBS --> other collaborative care

communication system → ex) that on pt only allowed to blink left eye Eye care → moisten eyes and keep lubricated Intermittent vs Indwelling Catheter paralysis = can't urinate appropriately Physical Therapy Nutrition may need to consider enteral feedings Psychological Implications full cognitive ability

Interprofessional care VTE -intermittent pneumatic compression devices (IPCs) -goal -how it works -need what assessment -when not worn

compress calf and or thigh goal→ improve venous return by the means of an electrical pump -like the compression stocking need to make sure they fit properly need skin assessment (removed q shift and look for skin breakdown) -need to be worn consistantly --> exceptions bathing, ambulation and skin assessment -not worn when active VTE --> risk for PE

INTERPROFESSIONAL CARE -compression --> explain // what also to look for -wound care --> what kind of dressing // and how to care for wound// what else do you do for the wound -nutritional status --> what kind of foods -antibiotic therapy

compression→ so many different types sometimes put a wrap of ace bandages many different types need to assess ABI to r/o PAD ABI 0.4 or less should not have compression stockings --->to rule out PAD wound care Clean wound Regularly moist environment dressings for ulcers hydrocolloid hydrogels → used by either wound care specialists or plastic surgeon Assess wounds for signs of infection culture and antibiotics only when needed Debridement, wound excision, skin grafting Nutrition high protein, Vitamin A, Vitamin C (fruits) and Zinc (meat and seafood) adequate calories and protein help with healing -pts with dm maintain adequate BS antibiotic therapy? - not routinely given, need to look for the clinical signs of infection (odor, pus, rthyema, color, changes in sensation, pain, warth edema etc) -therapy guided by the cultures and topical is not recommended

DRUG THERAPY MS -other types

corticosteroids Plasma Exchange (plasmapheresis) IV immunoglobulin G -bottom two are second-line tx for steroid resistant excerabations

MS --> interprofessional care -what are we treating

currently there is no cure for MS Collaborative care is aimed at treating the disease process and providing symptomatic relief Therapy is tailored specifically to the disease pattern and manifestations that the patient is experiencing → more symptoms = more therapies

at the scene immobilize

tell the pt to remain flat and in alighnement → keep legs straight can hold head always talking to them and someone call ems EMS use a backboard , collar, velcro head to backboard

Bowel Management -what can we do to not get them constipated -nursing dx -what is digital stimulation

digital stimulation--> ate breakfast and good place for bowel movement --> put glove on lubricate fingers and go up to anus and stimulate bowel movement // paristalsis--> then bed pan or commode Valsalva maneuver--> exert and bear down suppositories--> doglox, colace, stool softners enemas--> not frequently high fiber diet adequate fluid intake activity--> OOB regular schedule, e.g., 30" after brkfst*** upright position nursing dx knowledge deficiency and constipation

endothelial injury

direct injury or indirect injury direct surgery, fracture of pelvis leg or hip, hx of previous embolus, central line or catheter → fibrin clots form at the end of them indirect: dm, chemo, sepsis damaged endothelium stimulates: release of clotting factors, activation of platelets

RHIZOTOMY -max beneficial when after pro cedure -last how long -def

disabling the sensory nerve at the facet joint -severing or ablation maximum benefit from this procedure is typically experienced about 2 weeks afterwards, and this typically lasts 8-12 months may need to redue it at different sections

Gardner-Wells tongs

device for immobilization of cervical spine injuries in which two sharp metal pins are screwed into the superficial layer of the skull. they are then connected to hang in weights or other traction devices for stabilization of the spine. they may also be used for definitive treatment of spine injuries. * halo around head that uses traction --> device on bedside *use weights and this helps straighten out vertebrae *allows spinal cord for more room and increase healing usual out the pounds according to level 5 each *temporarily until surgery *realigns and reduces vertebral instability

Complications of PD * dysphagia --> * generally debilitating --> can lead to these infections * orthostatic Hypotension

dysphagia malnutrition aspiration important to know the s/s and on the correct diet General Debilitation pneumonia UTIs Skin Breakdown→ turn q 2 hrs Orthostatic Hypotension falls and injuries Sleep Disorders Quality of life Non-motor Symptoms depression, anxiety, apathy

What women are at risk for VTE formation (hypercoagulability)

estrogen based oral contraceptions smoking pregnant postmenopausal women over 35 fam history

PT W/ MS MUST NEED WHAT TO BE DIAGNOSED (3)

evidence of at least 2 inflammatory demyelinating lesions in at least 2 different locations within the CNS Damage or an attack occurring at different times (usually >/= 1 month apart) All other possible diagnosis must have been rules out

PD --> etiology

exact cause is unknown -may be from some genetic sand environmental issues

bradykinesia

extreme slowness in movement

TREMOR

first sign may be minimal --> only the pt notices at first -can affect handwriting -more prominent at rest -agravated by stress and increase concentration "pill rolling"--> thumb and forefinger move in a rotary fashion like rolling a pill or other small object -can also involve the diaphragm, tongue, lips and jaw but rarely causes shaking of head

Anticoagulation therapy for VTE TREATMENT (pts with confirmed VTE)

for confirmed VTE patients should receive: LMWH, UH or an oral Factor Xa drug -oral VKA also may be considered --> a INR of b/w 2-3 will be maintained active treatment for VTE should continue for at least 3 months * patients with co-morbidities, a very large VTE or other complex medical issues are hospitalized for treatment *** use parental UH

Myasthenia Gravis --> MANIS * hallmark

hallmark= **SPECIFIC SKELETAL MUSCLE WEAKNESS THAT FLUCTUATES** strongest in the morning and evening become exhasuted affects mutliple muscle groups ocular motor disturbances (⅔) ptosis → drooping of eyelid difficulty chewing, swallowing, talking or BREATHING ONSET --> only ocular motor muscles involved for about 50% of patients--> bilaterla ptosis or transient diplopia

CLICKER - Your patient is lightheaded while sitting OOB. What would you do? A. check his blood pressure B. lay him down C. administer fluids D. assess his Glasgow Coma Scale

he is talking so dont bother with glascow dont know whats going on wont give fluids right away check BP and see how it is

Intrathecal Baclofen Pump

help treat stiff muscles and spasms into the intrathecal area (near spine)--> pump in abdominal and cath in the spinal area → releases medication to help with muscle spasms seen in chronic patients with severe spascity → where reg meds do not work

common long-term disabilities

hemiparesis inability to walk complete or partial dependence of adls aphasia depression stroke is a life long change or families and survivors

WHAT IS THE MAJOR CAUSE OF HEMORRHAGIC STROKE? (3)

high BP → HTN also heavy lifting/straining clients who are on blood thinners

Intracerebral Hemorrhage

high mortality → where located and less access to perform the usually treatments and therapys 40-80% mortality rates most common cause is HTN other causes: coagulation disorders, anticoagulant and thrombolytic therapy, trauma, brain tumors and ruptured aneurysms Bleeding is from BLOOD VESSELS WITHIN THE BRAIN → really deep (usually in basal ganglia) commonly occurs during period of activity Sudden onset of symptoms --. progression is minutes to hours b/c bleeding change in LOC Headache Vomiting depending on amount, location and duration of bleeding → neurologic deficits blood clot within the closed skull puts pressure and displaces brain tissue, and decreases cerebral blood flow

DRUG THERAPY --> direct thrombin inhibitors * classified as what (2)

hirudin derivatives or synthetic thrombin inhibitors action --> binds specifically with thrombin without causing platelet protein and platelet intercations

GBS --> Diagnostic studies

history and physical → S/S Csf elevated protein abnormal EMG MRI to rule out other causes

Carotid endarectomy -what is it -when do you do it -what is important post-op

if patient has had hemispheric symptoms in the past 6 months and more than 50% ICA stenosis, or more than 60% ICA stenosis in an asymptomatic patient removing the plaque build up to improve blood flow removing plaque from the arteries and lowers chance for smoke makes an incision in the neck and open the carotid artery and remove that plaque and shunt may be put in what is important post - op period AIRWAY PROTECTION → if have inflammation → blocks this evuluate ABCs excessive bruisng or bleeding

PE --> RISK FACTORS

immobility -muscle contraction is what is pushing the blood back to the heart surgery -at risk for bleeding history of VTE Cancer -stimulation of the body to make more substances like clotting factors - chemo can damage walls of blood vessels and put them at higher risk Obesity Oral contraceptives Pregnancy -less blood flow to legs in later preg -also pelvic blood vessels are compressed Clotting Disorder -many different kinds

akinesia

inability to initiate movement, absence or loss of control of voluntary muscle movements and brady is th slowness of movements -stooped posture, drooling saliva, shuffling gait

Rigidity

increase in muscle tone at rest characterized by increased resistance to passive stretch

Rigidity

increase resistance to passive motion when the limbs are moved through their range of motion -jerky quality -intermittent catches in the joint caused by sustain muscle contractions pts complain of muscle soreness, pain in head, upper body, spine, legs

DRUG THERAPY --> THROMBIN INHIBITORS -2 types

indirect --> UH and LMWH direct -->Argatroban and Hirudan Dabigatran (Pradaxa)

MG NURSING DIAGNOSIS

ineffective airway clearance → meds can cause increase secretions impaired verbal communication (weak ness of face) impaired swallowing activity intolerance (r/t muscle weakness and fatigubility) disturbed body image → facial muscle loss, drooping of eye

MS -precipitating factors

infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, poor state of health

NURSING IMPLEMENTATION for VTE

interventions to prevent complications with patients receiving anticoagulants Guaiac stool/NG specimens -use the card → pull out activator -if see any blood indicated blood in stool -let provider know and monitor the pt for s/s of beeding Eval for S/Sx bleeding (increased HR, RR, low BP) -tahycardiac, hypotensive, tachpnic Assess for hematoma/ecchymosis -hematoma→ underneath skin (seen commonly in abdomen) -ecchymosis→ if getting SQ injection abdomen can become eccymotic → repeated injury Minimize venipunctures (use small gauge) for IVs Avoid IM injections if on anticoagulants Apply manual pressure for 10 min to venipuncture sites -ex) when pulling out an IV, blood draw→ if on anticoagulants -could have blood across room, gauze saturated with blood -in order that achieve hemeostasis Use electric razor→ not straight razor Humidify oxygen→ helps minimize irritation 02 is drying → risk for bleeding in nose Apply moisturizing cream -prevent cracks Stool softener -soft stool if not cause more probelms // rectal bleeding Avoid wearing tight clothes when traveling long distance exercise calf muscles, short walks, non-alcoholic or caffiene bev.

PE DIAGNOSTIC STUDIES - labs to be drawn (2)

labs D-DIMER neither specific or sensitive fibrin degregation product elevated → do more diagnostic studies (pts with small emboli may have normal results) ABGs Chest X-ray quick and easy ruling out other disease processes EKG may see sinus tachy right heart strain → may see changes in the T wave Echocardiogram ultrasound of heart → looking for right heart strain

cerebral blood flow -def -how much o2 and glucose does brian use

is the amount of blood in ml passing through 100 g of brain tissue in one minute 02--> 20% glucose 25%

pathophysiology of thrombus formation

localized platelet aggreation (esp. at vein valve cusps) and clotting factors that stimulate fibrin ENTRAP RBCs, WBCs, and platelets and begin to adhere to vein wall --> thrombus formation --> as thrombus grow forms a tail that can eventually block the lumen --> risk for embolus formation with turbulent blood flow

sympathetic nervous system -where located

located in between T1 and L4 * loss of temp control, loss of vessels response * edema can extend up and down on spinal cord

look over the brain structure

look over the brain levels

MS PATHO -what initially happens

loss of myelin Sheaths no nerve damage no loss of function some possible slowing myelin can regenerate → can lead to remission phase of MS

MS Evaluation

maintain or improve muscle strength and mobility. Use assistive devices appropriately for ambulation and mobility.--> can, walker, wheelchair Maintain urinary continence. pelvic floor activities Make decisions about lifestyle modifications to manage MS.

Interprofessional care VTE -identify high risk pts

mandated by the joint commision need to identify these pts who is high risk?? immobile, surgery, new med (hypercoagulability), current drugs, past medical history, high bleeding/thrombsis risk

PD NURSING MANAGEMENT --> planning

maximize neurologic function maintain independence in activities of daily living (ADLs) for as long as possible feed dress bathe Optimize psychosocial well-being Avoid complications such as contractures and falls gait instability → high risk for falls collaborate and support caregivers who may also experience stress associated with disease progression (ex-dementia)

Metoclopramide (reglan)

may be used to treat delayed gastric emptying.

MS DRUG THERAPY --> what are they used to do -what types

medications are used to treat relapses, manage symptoms and slow the progression of disease Immunomodulators

Neurologic examination -mental status? -pupil (acronym, document) -cranial nerve function -cerebral function -reflex -motor and sensory function

mental status→ alert oriented, know where they are, who is pres, count backward level of consciousness (LOC)--> x3→ ask each one if have a change → document this in your notes and explain Pupils what acronym → PERRLA → pupils equal, round and reactive to light with accommodation pupil reaction, room should be dark → take it from the side to center of eye → note if it is BRISK VS SLUGGISH, note the size of the eye anisocoria→ unequal pupils → these can be normal for people document if they have a lens → these people will not have a normal reaction time cranial nerve function→ need to KNOW, on next slides cerebellar function (balance and coordination)--> ROMBERG'S TEST → close eyes with arms up → if the arm drifts down → say positive drift on the right reflexes→ cough if put something in mouth corneal reflex, gag reflex , deep tendon reflex motor and sensory function→ look over grading, compare side to side*** also remember that they may be being asked these questions over and over again so may not even know the right answer but state the right answer because have been asked it so frequently

CT angiography (CTA)**

most common test to diagnose PE uses IV injection of contrast dye → allows for visualization of the blood vessels to see where clot is What do we need to know before administration of the DYE? RENAL FUNCTION if in CKD → dye is metabolized by the kidneys if give them this dye the kidneys won't be able t metabolize it and go into renal failure dialysis patient → cna pair it up with dialysis tx so can get washed off

Clinically isolated syndrome

must last at least 24 hours Characteristics of MS but does not meet criteria-precursor ** first symptom of the demyelination when people have they may or may not develop it accompanied by a lesion on the brain → highly likely that will have MS

DIFFERENCE BETWEEN MYASTHENIA AND CHOLINERGIC CRISIS * what are the definitions * what tests --> results of the tests

myasthenia gravis crisis → due to worsening of the feature cholinergic crisis occurs when there is too much anticholinesterase drug which causes an increase in acetylcholine at the receptor sites usually occurs w/in one hour after taking anticholinesterase drug Give EDROPHONIUM test to tell the difference→ TENSILON If symptoms improve then myasthenia crisis if they worsen than Cholinergic crisis

Transluminal angioplasty -with possible stenting

narrowing of vessel → so open vessel up and apply a balloon to improve blood flow usually through femoral or radial and thread it up to the carotid WHAT IS POST OP IMPORTANT neurovascular checks → if through femoral → need to look at the legs (pulses, cap refill, warm) Goal is to maintain patency of the artery Done with during angioplasty Post-operative includes: Neurovascular BP management Bleeding

Drug therapy --> INfusions * 3 types * used for what kind of MS

natalizumab (Tysabri)--> ---> given when they have no other response to the other drugs// but have potential for a serious infection leukoencephalopathy mitoxantrone (Novantrone)-antineoplastic Dimethyl fumarate (Tecfidera) typically have MANY severe side effects, not the first line of defence, used in a very active disease process that traditional therapies not working on

MS --> SURGICAL MANAGEMENT

neurectomy → removing part of a nerve, for severe chronic pain Rhizotomy → when the surgeon cuts part of spinal nerve, goal is relieve muscle tension Cordotomy → disables selected pain reduction tracts, disconnect pain

How would you know if the patient is having complications from Thrombolytics?

neuro assessment → if they start bleeding in the brain → will have worsening symptoms (may not take that long) cushings triad, widening pulse pressure etc → may have converted to ischemic to hemorrhagic why it is so important to admit to an ICU→ so csn do frequent neuro checks and oick up on the symptoms quickly

Interprofessional care of PD * focus on what DRUG THERAPY * aimed at what * actions (2)

no cure → focus on symptom management Drug therapy aimed at correcting imbalances of neurotransmitters within CNS Antiparkinsonian drugs either *****enhance // release supply of DA ******Antagonize or block the effects of overactive cholinergic neurons in the striatum (that release Acetylcholine) dopa or anticholinergic

PE COMPLICATION -Pulmonary HTN

occurs form hypoxia usually with recurrent PEs*** ( rare if you have just one) high bp that affects arteries in the lungs from the right side of the heart being strained*** not in a acute process arteries become stiff and thick

TRANSIENT ISCHEMIC ATTACK -def -how long it lasts -____ sign

occurs when blood supply to part of the brain is blocked→ whatever is causing this blockage → warning sign of progressive vascular disease depending on where in the brain is ischemic anterior cerebral artery middle cerebral artery internal carotid artery Transient episode of neurologic dysfunction Symptoms last less than 1 hour Warning sign--> may be from the microemboli blocking

Dorsal Column Electrical Stimulation

on or two electrodes are introduced in the epidural space in the mid thoracic area → allows impulses to be generated which activates this electric tip in epidural space which hopefully blocks some of the symptoms to reduce pain

PD --> clinical manis * onset

onset is gradual and insidious -initially only one side may be involved classic triad of PD TREMOR mild at first (may only noticible to pt) affects handwriting most prominent at rest described as "pill rolling"--> thumb and forefinger RIGIDITY→ increased risistance to passive range of motion jerky quality Bradykinesia → slowness of movement occurs do to changes in basal ganglia

MS -clinical manis * onset * initial symptoms

onset is slow and gradual symptoms often vague that happen months/years each patient is unique and not everyone will have the same symptoms--> according to area of CNS involved ex) some people very minimal all the way to wheelchair or vent support -can either be chronically progressive or relapsing // remissions--> however overall trend is progressive deterioation

L1 injury

paraplegia, results in paralysis below the waist -bladder problem

C6 injury

partial paralysis of hands and arms as well as lower body -having some muscle ability and sensation --> may be helpful --> more control over environement

MS --> collaborative care -speech therpay and physical theraoy

physical Therapy relieve spasticity improve coordination Train patient to substitute unaffected muscles for impaired muscles. Water exercise→ helps give bouyancy to the body → that allows for movement that generally isn't possible Nursing Diagnosis: Impaired Physical Mobility Speech Therapy dysphagia, dysarthia

GUILLAIN - BARRE Syndrome * de f * occurs when

polyneuropathy in which the body's immune system attacks the myelin sheath of the PNS Usually occurs after a viral or bacterial infection (acute inflammatory demyelinating polyneuropathy → AIDP)

MG --> exacerbation (precipitating factors) -also what drugs cause exacerbation

precipitating Factors: emotional stress fatigue pregnancy/menses trauma temperature extremes hypokalemia adverse medication reactions Aminoglycoside Antibiotics→ genomysin Beta Blockers Procainamide Phenytoin → seizure med Psychotropics tricyclic antidepressants Benzodiazapines Lithium Carbonate Neuromuscular Blockers

VENOUS THROMBOEMBOLISM (VTE) -what does this term account for -DVT --> what does it stand for (3)

preferred terminology accounts for deep vein thrombosis (DVT) to pulmonary embolism DVT: thrombus in a deep vein iliac femoral popliteal normal blood flow→ blood starts to collect (form new BC, or some injury to that area)--> then become dislodged and travel

ASSESSING FOR POSTURAL INSTABILITY

pt may state unable to stop themselves from going forward or backward Can do the PULL TEST remember safety stand behind pt and tug backward on the shoulder scale of 1-4

VTE : SURGICAL INTERVENTIONS -venous thromboectcomy

rare involves the removal of a thrombus through an incision of the vein anticoagulant therapy is recommended

Amyotrophic Lateral Sclerosis * def // loss of what * also known as * onset * life expectancy after diagnosis

rare progressive neuromuscular disorder loss of motor neurons in the brainstem and spinal cord that control voluntary muscles known and LOU GEHRIG disease Onset 40-60 years of life Life expectancy is 2-5 years after diagnosis ALS is a motor neuron disorder → remember motor neurons are essential for communication between the brain and voluntary muscles → both the upper /lower neurons degenerate or die and stop sending messages to the muscles in ALS

Reflexes

return of reflexes may complicate the rehabilitation * hyperactive *exaggerate responses *penile erections * spasms (after period of spinal shocks) - patient or family may see this as a return but it is not controlled by brain may be spinal impulses --> NEED TO EXPLAIN THIS Inform the patient of the positive use of these reflexes in sexual, bowel, and bladder retraining. Spasms may be controlled with the use of antispasmodic drugs. Most commonly prescribed are baclofen (Lioresal), dantrolene (Dantrium), and tizanidine (Zanaflex). Botulinum toxin injections may also be given to treat severe spasticity.

COMPLICATIONS OF PE (3)

right heart strain Pulmonary HTN Pulmonary infarction

Interprofessional care -_> preventative therapy

risk control factors (think back to risk factors) reducing their sodium , low in fat, exercise, smoking cessation, limt alcohol and BP managment

Subarachnoid Hemorrhage

ruptured of cerebral aneurysm bleeding into the cerebral spinal fluid-filled space between the arachniod and pia matter may not have warning signs→ viewed as the "silent killer" s/s → depends on severity of the bleed may have people that are alert or comatose Complications rebleeding before surgery or other therapy is initiated cerebral vasospasm

acute subdural hematoma

s/s in 24-48 hours Decreasing LOC and headache Size determines clinical presentation and prognosis Ipsilateral pupil may become fixed Cerebral edema

what do we need to montior if have a cath in head

s/s of infection!!→ needs to be very sterile -need to also monitor the amount of CSF --> make sure there is sign with the patient to be careful when moving turning feeding etc of the aptient --> do not want to lose too much -drainage can be continuous or intermittent

OTHER DRUGS -MAOI inhibitors * 2 names * action * less effective in what

selegiline and rasagiline, may be combined with Sinemet to block DA breakdown. -increase DA and prolong the half-life of levodopa -less effective in treating motor symptoms than DA receptor antagonists

UNFRACTIONATED HEPARIN (HEPARIN) -major side effect

site effect → bleeding, heparin Induced thrombocytopenia (HIT)--> immune reaction to heparin → dramatically reduces platelet count along with paradoxical increase in arterial and venous thrombosis ex) someone comes in platelet count was 350 and now 70 b/c put on heparin→ work up for HIT HIT is *diagnosed by measuring heparin antibodies TX OF HIT --> immediately stopping heparin and if further anticoagulation therapy is required and using a non heparin anticoagulant another long-term se --> osteoporosis

Primary Progressive MS

steady and gradual deterioration, no acute attacks * less than 10% pts diagnosed individuals who were previously diagnosed with progressive-relapsing MS would now be considered primary progressive: active (at the time of relapse or new MRI lesions) or not active (new guidelines) → steady decline upward not as many ups and downs

ENDOVASCULAR THERAPY // CLOT REMOVAL -explain the procedure -the amount of time

stent into the artery with a blood clot → the stent expands and allows the blood to flow → the clot goes into the stent and the clot is removed → helps open blocked arteries in the brain Mechanical thrombectomy for patients with large vessel occlusion within 6 hours of stroke onset Tpa is 3-4.5 this is is 6 hours Open blocked arteries in the brain Many different types of stent retrievers available

Cushing's Triad

systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and irregular respirations -medical emergency b/c sign of brainstem compression and impending death

quad coughing

take deep breathe and cough--> nurse takes her fist into the diaphragm to increase the thoracic pressure and hopefully help increase the secretions

CEREBRAL BLOOD FLOW -cerebral autoregulation -what does increase CO2 do -collateral circulation -ICP

the brain needs a constant supply of blood flow to provide O2 → cerebral Blood Flow blood flow must maintain 750-1000 mL/min or 20% of optimal CO for optimal brain functioning if blood flow is completely obstructed → neurologic metabolism is altered in 30 seconds, metabolism stops in 2 minutes, and cerebral death occurs in 5 mintues CEREBRAL AUTO REGULATION→ systemic arterial BP is well protected and kept in a range of 50-150 mmHg involves change sof cerebral blood vessels in resposne to changes in pressure so blood flow to the brain stays constant when ischmeia occurs cerebral autoregulation may be impaired making the brain dependent on systemic BP Co2 is a potent vasodilator → therefore changes in arterial CO2 have a dramatic effect on cerebral blood flow factors that affect blood flow to the brain include systemic BP, CO anbd blood viscosity cardiac output has to be diminished by at least ⅓ before cerebral blood flow can is reduced COLLATERAL CIRCULATION→ may develop over time to compensate for a decrease in cerebral blood flow an area of the brain can recieve blood from another vessel if the OG vessels is cut off "alternate route" ICP → also influences cerebral blood flow increase ICP → causes brain compression and reduced cerebral blood flow

TIA involving the vertebrobasilar system

tinnitus vertigo darkened // blurred vision diplopia ptosis dysarthia dysphagia ataxia unilater/bilateral weakness/numbness

Cerebral aneurysm clipping

tiny clamp at base of aneurysm to stop blood flow → keeps it from bursting or recently hemorrhaging from hemorrhaging again shrival up b/c not getting o2 and blood supply that it needs

Parkinson's disease pathophysiology

top of graph is normal and the bottom is missing a step (we want to see the balance of DA and Ach --> normla person the inhibitory effects of DA are balanced by the excititory actions of Ach and controlled movement results the neurons in the substantia nigra that supply the dopamine degenerate → leads to deficiet of dopamine and the excititory effects of acytlcholine***** DA < Ach--> and unopposed//disturbed movement results

VENOUS ULCERS COMPLICATIONS -complications -where is it most commonly seen

typical above medial malleolus / near Lateral Malleolus Irregular wound margins ruddy tissue partial thickness wound extend through epidermis and some dermis drainage may be extensive pain worse when leg dependent infection and cellulitis if untreated severe complications --> osteomyelitis and malignant changes may need amputation

Carotid Duplex Screening (stroke diagnostic)

typically done once they get admitted → ultrasound of the carotids and assessing blood flow through the carotids if have a stenosis or athersclerosis → you are cutting off major bloood supply to the brain and not getting perfusion thats necessary

upper motor neuron vs lower motor neuron

upper --> from brain to spinal cord --> consiously control movement lower --> spinal cord to muscle --> do not control them all the time c2 lesion --> even though cannot consciously control --> the spinal cord may still send signals --> still have spastic valve and bladder increase risk for VTE --> this is why this may be a good thing

VTE DIAGNOSTIC STUDIES non-invasive venous study

venous duplex ultrasound → evaluates the blood flow in the arteries and the veins → red arterial blue venous -combination of compression ultrasound and spectral color flow doppler --> veins examined for compressability and intraluminal filling defects to help determine location and extent of thrombus *** **most widely used test to detect**

Interprofessional care VTE -early mobilization

we want them up, if on bed rest q2 hrs ambulate 4-6x a day (use gate belt) OOB for meals--> ie in a chair -early and aggressive mobilization based on the pts condition is the most effective and cost benefit tx -early and frequent is sufficient for low risk VTE pts -unless contraindicated --> teach pts to flex and extend their knees, feet and hips every 2-4 hours

MS MANIS -motor

weakness and paralysis of limbs, trunk head--> problems with coordination and balance Leg spasms diplopia → double vision dysarthria, scanning speech spascity→ refers to stiffness, and wide range of muscle spasms bent wrist closed fist relaxed elbow

Monroe Kelly hypothesis

•*Reciprocal relationship* occurs between all of the intracranial components •Small* increase in volume of one component* can be compensated for by a *decrease in the volume* of one or both of the other two components. •*Venous compression* will displace volume - if any component increases (brain tissue with lesion, cerebral bleed, hydrocephalus for example), one of the other components will decrease/compensate

Modifiable Risk Factors

→ 90% are caused by this Review risks Hypertension***** Undetected and untreated if proper tx of HTN can reduce risk of stroke by 50% Atrial fibrillation ~25% of strokes → quivering of the atria → if in left atria → will be pumped out into the systemic system and see if become a stroke other heart disease DM--> 5x higher than general pop. smoking --> doubles the risk for ischemic stroke, decreases substantially after the smoker quits, after 5-10 years have the same risk as non smokers alcohol--> depending on amount consumed illicit drug use stress increase waist circumference women who experience migraine with aura PHYSICAL inactivity early forms of birth control pills

COMPLICATIONS OF ICP **BRAIN DEATH -def -what wont we see -what test is perfromed -what do we need done to confirm this

→ absent of perfusion to the brain Once brain stem problem is when we see the decrease in other vital signs absence of movement, response to pain No corneal, gag(even with suction), cough(even with tongue depressor), or pupillary reflex(large but no response) Apnea despite elevated pCO2 when removed from the ventilator (oxygen flow by only) Apnea test → 60 to 100 % o2 with out a ventilator giving them breathe Can also do doppler carbrain to look for perfusion NEED 2 separate exams by 2 SEPARATE providers→ to check for brain death in DE Reason for this → take them off the ventilator

Fingolimod (Gilenya)

→ also antiinflammatory properties → but ALSO has SE of BRADYCARDIA → which limits the the cells from going back to CNS → goes back to the T cells and preventing from causing damage -tretament of relapsing forms of MS

BASILAR SKULL FRACTURE

→ base of skull Raccoon's eyes → blood around orbits (edema and ecchymosis) Battle sign → behind ear on mastoid process Otorrhea, rhinorrhea→ CSF from ear and draining from nose → sometimes so bloody do not know if just bleeding or csf Can also check for glucose → however you do not know if elevated glucose for stress/ DM → therefore halo sign is better to tell Halo or ring sign CSF is the ring / halo around the blood Depending if anterior, middle or posterior fossa of base of skull is fractured will change your s/s Halo sign is better than checking sugar content of CSF - if patient diabetic or under stress, CSF may contain elevated amts of glucose.

OCULOCEPHALIC RESPONSE -other name -what is the normal rx and what is abnormal

→ doll's eyes ABSENCE → not with spinal cord injury b/c moving the head Normal Reaction→ should be positive → when the head is moved from side to side the eyes should move in the opposite direction They should understand doll's eyes and cold calorics Careful if c-spine injury - then logroll side to side rather than turn head!****** Want the rxn→ think about a very expensive doll the eyes will move → a dollar store doll will not move this is negative → we do not want this

conjugate gaze deviation

→ frontal lobe lesion→ includes cranial nerves 3, 4,6→ have them follow finger in H motion and make sure the eyes move together → note where the eye is going ex) deviating to up and left

MS MANIS -bladder -what kind of bladder leads to what (2) -what is the treatment

→ goes back to ms lesions → block or delay transmission of nerves that go to the bladder Constipation Spastic Bladder small capacity = incontinence Flaccid Bladder Large capacity + no sensation = incontinence intermittent self-catheterization (sometimes need chronic foley or suprapubic cath) pelvic floor physical therapy → trying to strengthen pelvic floor muscle contorl and relaxation both flaccid and spastic increase risk for UTIs

mechanism of injury

→ inorder to see what the possibel injurues are common one is flexion and extension → ez) someone in a car → hit forwards and backwards from that motion get rupture of ligaments fractures and edema→ COUP // COUTRECOU compression fracture → clift diving ---> may have fractures compress the cords→ Flexion rotation → fallig of horse and twisting → compresion of cord AXIAL LOADING → pressure on landing on head and neck → excessive flexion and snapping cord

unilateral dilated pupil

→ is a sign of ICP→ cranial nerve 3 → compressed on the same side of the hematoma (ipsilateral)--> sluggish or not reacting

secondary injury

→ is the resulting hypoxia, ischemia, hypotension, edema, or increase ICP that follows the primary injury

Relapsing-remitting MS (RRMS)

→ most common ** (85% initially diagnosed this way) mild to moderate disease symptoms develop and then resolve in weeks to a few months (partial or complete recovery) Return to baseline status with recurring relapses, develop new symptoms *** eventually most people that have will move onto the secondary progression stage) → most common, relapse and then they build new symptoms as they baseline symptoms become worse and worse 85%

primary injury

→ occurs at the initial time of injury→ ex bullet, (blunt force, car accident, trauma)

positive papilledema

→ optic disk edema → use the ophthalmoscope***

irregular pupil

→ orbital trauma, lens implant → find out the other injurues

small pinpoint

→ pontine injury, opiate administration

plasma exchange or plasmapheresis

→ remove scirculating antibodies thought to be active during this acute flare up → research is still conflicting whether effective therapy or not

ICP system

→ to monitor and drain Schema showing with ventric can drain fluid/blood but turn the stopcock and can monitor pressure Mention that the MD/NP writes order to keep ICP/CPP at a certain value - may need to raise or lower ventric bag based on orders. Typically level to the Foramen of Monroe using level If bag too high - won't drain If bag too low - drain too much and can actually pull small vessels and cause bleed Goes to head , taped on the shoulder to make sure stays in → attached to the bag → drip chamber collecting They will make sure that the device is level → if you want to drain more drop lower

abnormal blood flow -other name -who is at risk

→ venous stasis (who is at risk for venous staisis?? bed rest, immobile,a fib, heart failure (bad contractility) postpartum, obesity, spinal cord injury, fractured hip dysfunctional vein valves, inactive extremity muscles, change in unidirectional blood flow