exam 3 Flashcards
(39 cards)
Fatal genetic disorder that causes progressive breakdown of nerve cells in the brain
Physical and mental abilities deteriorate over time
No cure
Ability to reason, walk and speak are affected
Affects entire brain, not just 1 area - caused by degeneration of nerve cells within brain
Is autosomal dominant - Genetic
Brain isn’t impaired, so trapped in own body
Family cares for them
NM:
-No treatment will alter the course of the disease
-Medications can help control symptoms of movement and psychiatric
-Medications that help with chorea:
–Tetrabenazine (Xenazine)
–Levetiracetam (Keppra) helps with involuntary movements
–Clonazepam (Klonopin)
-Antipsychotic drugs
–Quetiapine (Seroquel), risperidone (Risperdal) - can help depression but in some pts with HD can do opposite and make worse
-Goal: manage S/S and reserve quality of life
-Speech therapy
–Help with speech, eating, and swallowing
-PT/OT
–Safety, exercises to maintain strength, provide assistive devices for home, adaptive utensils for eating/drinking
-Psychotherapy
–Talk therapy, manage behavioral problems, coping strategies
Huntington’s Disease
Usually appear between 30-50 years of age Worsen over 10-25 year period -Personality changes, mood swings, and depression* -Forgetfulness and impaired judgment -Unsteady gait -Involuntary movements (chorea) -Slurred speech* -Difficulty swallowing* -Significant weight loss* -Dysponia ? unsteady? -uncoordinated jerkey movements Diagnosis -Physical examination --Neurological --Psychiatric --Family medical history -Clinical manifestations -CT or MRI – structural changes of brain – used for rule out -Genetic testing
Huntington’s disease 2
The immune system mistakenly attacks the peripheral nervous system
Acute inflammatory demyelinating polyneuropathy
Immune mediated neuropathy – Lymphocytes and macrophages strip myelin from axons
-Causes a loss of our nerve impulses being sent
Seen in PNS, cranial nerves, and spinal nerve roots
Disease follows GI/resp illness - Demyelination of nerves that control the diaphragm and intercostal muscles result in respiratory failure. Require mechanical ventilation.
- immune system is primed and cant recognize normal/abnormal and it attacks the nerves
Guillain-Barre Syndrome
Ascending* paralysis develops quickly: concern = lungs/ability to breath
-Ground to Head* – happens in lower extremities first
Symmetrical weakness & paralysis*
-Respirations, Bowel and bladder paralysis: bowel: paralytic ileus (sedment of bowel stops function) - cuts of stimulation -> ischemia necrosis; bladder: urinary retention -> pathogens -> UTI
-Swallowing, talking disrupted
-Sensory loss
Areflexia – absent or depressed - may progress to complete paralysis all all 4 limbs
Tenderness and Pain – due to exposed axons
Respiratory Compromise*
At risk pts: autoimmune disease (vaccinations (rabies) r/t activate immune system
Guillain-Barre Syndrome 2
Complete functional recovery can take up to 2 years for some people. Some may develop residual symptoms because the axons were damaged permanently after demyelination.
If the cranial nerves are affected – optic nerve demyelination can cause blindness. Become unable to swallow or clear secretions due to demyelination of vagus nerve and glossopharyngeal nerve.
DOES NOT affect cognition of LOC.
Diagnosis:
-Depends greatly on patient medical history & progression of symptoms
–GI or respiratory disorder 1-4 weeks earlier???
-Lumbar Puncture - not definitive
–Increased proteins* (found in only 50% of patients with early GBS) (late see 90% of time)
-Electromyography – nerve conduction study
-Pulmonary function tests to get baseline and anticipate progression
NM:
-Great risk for respiratory compromise
-DVT Prophylaxis
-Monitor cardiovascular system
–Telemetry, blood pressure
-Plasmapheresis: machine to clean plasma in body - central line double lumen needed to eat macrophages (prevents progression)
-IVIG
Concern = mobility (DVT heparin/lovenox, SCD) - PT/OT to preserve muscle function and prevent atrophy
NM:
-Neurological Assessments: see progression/plateau : reflexes/strength
-Cardiovascular Assessments: affects SNS big BP swings -> risk of dysrhythmias
-Respiratory Status
-Gastrointestinal and Urinary Function: bowel/UI retention
-Mobility – PT/OT will be huge!
-GOAL = Prevent infection and complications of immobility
-Aspiration Precautions
-Communication
-Respiratory Status
-Cardiac Monitoring
-Comfort Measures
-Psychosocial support
Guillain-Barre Syndrome 3
Caused by the unilateral inflammation of the facial nerve or cranial nerve VII
Results in weakness or paralysis of the facial muscle
Cause is unknown but theories include:
-Vascular ischemia: decrease blood supply to nerve
-Viral infections (herpes simplex, herpes zoster): virus
-Autoimmune disorders
nerve inflammation: not lack of sheath like others
Test: close eye against force
all 1 side: droop eyes (ptosis), corner mouth droops r/t muscle not working
Bell’s palsy
7th cranial nerve: smile, tongue, scrunch eye and face muscle
S/S:
-Unilateral facial paralysis
-Decreased lacrimation: stop making tears so dry eyes
-Painful sensations to the face: weird sensation like foot fell asleep
-Speech difficulties – decreased salivation: muscle to make lip/jaw move is compromised
-“Mask like” appearance of affected side: can’t move 1/2 of face
NM:
-Corticosteroid therapy
-Antiviral medications
-Analgesics for pain
–Heat can be applied to aid circulation
-*Protect affected eye from injury and corneal ulcerations: eye patch/shield r/t muscle can’t hold eye closed - give eye drops r/t decrease tear/dry eyes to preserve eye function
Bell’s Palsy 2
Chronic pain condition that affects the trigeminal or cranial nerve V
AKA tic douloureux
Form of neuropathic pain
Causes: Variety of conditions
-Blood vessel pressing on trigeminal nerve -> compression which cause pain - surgery to cut out blood
-MS patient – deterioration of nerves myelin sheath
-Injury to the nerve – sinus/oral surgery, stroke, facial trauma: car accident, surgery where nerve was nicked/cut
Extremely painful - 1 side
-Hallmark S/S: acute pain on 1 side of face
Trigeminal Neuralgia - 5th cranial nerve
S/S:
-Intense flashes of pain
–Extreme, sporadic, sudden burning
–Shock-like facial pain
—Can last seconds to minutes
–Aching, burning, stabbing pain (neurologic pain)
-Pain can be triggered by vibration or contact
–Brushing teeth, eating, drinking, talking, exposed to the wind
Diagnosis:
-History
-Clinical manifestations
-Physical & Neurological assessments
-Rule out other causes
–Shingles (activated by herpes), headaches/migraines, TMJ
-Diagnosis can be difficult
-MRI – rule out tumor, check for nerve compression (check to see if something is there they can remove it)
-No test/lab - must rule out, check progression and S/S
trigeminal neuralgia - 5th cranial nerve
Eye, cheek, jaw
sensation effects it (trigger)
trigger sets off pain - can be above or below or side (depends what nerve it effects)
Treatment:
-Anticonvulsant medications – block nerve firing
-Tricyclic antidepressants – help treat pain
-Surgery:
–Rhizotomy – nerve fibers damaged to block pain (meant to kill nerve with probe/electrical currents - for syatic/low back pain)
—Balloon compression – pain relief only lasts 1-2 years (push blood supply away from nerve)
—Gylcerol injection (kills nerve root - med to damage nerve ending to stop sending signal)
-Depression/isolation
-Sleep disturbances
-Non-pharmacological methods
NM:
-Ways to manage the pain using non-pharmacological methods to avoid triggers
–Chew food on unaffected side
–Rinse mouth when using a toothbrush is too painful
–Limit touch to face when possible
–Eat room temperature food
–Extreme hot or cold can cause increased pain
trigeminal neuralgia - 5th cranial nerve
Declining rates- more than 50%
70% burn injuries are men on hands/mouth from electrical wires
Average size is 10% TBSA
½ of patients are treated at specialized centers- less hospitalizations to prevent infection and keep segregated from others
Classifications: causative agent, depth, severity
burns
Thermal (temp/direct heat)
-70% of injuries
-Can be flame, explosion, scald, steam, or heat transfer via object
Chemical
-Exposure to acids and alkali (bleach)
-Contact time is critical*
-Will continue to burn as long it’s on skin
*Wash/flush up to 3 hours (reversal agents can –> complications) *wash it
Electrical (current moves through you - entrance/exit)
-Type of current is important (alternating or direct)
-Low voltage common with electrical cords on hands and in mouths (especially children) - Concentrated at point of burn
-For high voltage, look for entrance and exit wounds, leathery appearance, muscle flexion/contractures (claw like)
causative agent classification for burn
Factors include: -Temperature of the agent -Duration of the exposure -Areas of body exposed Discussed in terms of superficial (1st), partial-thickness (2nd), full-thickness (3rd) Table 53-1, pg 1186
depth classification for burn
Epidermal layer only- minimal intervention needed
Painful, then itches
3-5 days of healing, no scarring
-Skin might not be broken, heals itself in 3-5 days, no scars, starts painful/sore but skin still blanches
Treat: aloe, ice, Tylenol/ibuprofen, or lidocaine with aloe
superficial burns (1st degree) in depth classification
Superficial vs deep
Superficial: epidermal and top of dermal layers (minimal intervention, 10-14 days healing)
-Blister (don’t squeeze it), heal itself in 10 days-2 weeks, tissue regenerates
-Treat: Neosporin, soap/water, ointment, voer it, non-adheasive, keep granulated tissue separate
Deep: all of epidermis, lots of dermis. Consider fluids, nutrition, comorbidities
Deep partial-thickness burns require surgery if size is significant
-higher risk for infection
-IND to cut out old/dirty tissue, skin graft or silvidene cream
-hydrate, nutrition, protein to help rebuilt tissue
partial thickness (2nd degree) in depth classification
Extends to adipose tissue- why is this tissue concerning for healing?
Look white, red, brown, black- may see thrombosed vessels in top layers
Nutrition, infection
-Inside wound: not painful r/t destruction of nerves r/t pressure, but is painful outside the burn
-no regeneration r/t destroyed sweat glands and hair follicles
full thickness burns (3rd degree) depth classification
Consider:
Percentage of BSA burned (20%=burn center)
Depth
Anatomical location (perineal groin area is the worst)
Age (young health but larger BSA; elderly have delayed healing and risk for falls/decrease sensation)
Medical history (diabetes - pt with diagnosis is worse than normal patient)
Concomitant injury
Inhalation injury (lung damage r/t chemicals, steam, smoke and higher mortality)
classification : severity for burns
Estimation of nines or rule of palms
-Head 4.5
-Arm: 4.5
-Chest: 9
-Stomach: 9
-Groin: 1
-Legs: 9
all front and back and not good for infants
Palm = 1% of BSA and good for small scattered burns
Lund and Browder: better of measuring, time intensive, complete after patient is stabilized
methods of measurement for burns
- Activity at the cellular level->coagulation, local production of complement, histamine, oxygen free radicals (byproducts)->alters the cell membranes->increases permeability of vasculature (cell membrane becomes permeable for fluid and bacteria)
- Increased vascular permeability-> loss of plasma proteins to interstitium=decrease in circulating volume=interstitial edema (24-48 hours into the injury) (fluid shift -> lack of circulating volume -> decrease CO -> damage to internal organs like GI, brain)
- All of this affects the pulmonary vasculature, leading to pulmonary interstitial edema and intraalveolar hemorrhages->ARDS (lung injury along with hypotension/fluid volume -> ARDS)
This injury triggers the release of vasoactive agents all over the body->SIRS-> depletes intravascular volume->leads to organ damage-> hypovolemic shock->metabolic acidosis, hyperkalemia
Other systemic effects:
-increased GI permeability= increase in bacterial infections (r/t sirs so NG tube)
-Platelet and blood cell activation = inflammation->vasodilation->hypotension
-Prostaglandin activation= vasoconstriction->increased blood flow-> fever
-Circulating byproducts->lung, GI, and kidney injury; hyperglycemia followed by hypoglycemia; hypotension, metabolic acidosis, coagulopathy and activation of the coagulopathy cascade
-Resultant coagulation->thrombi->ischemia->necrosis
Stress response can cause peripheral vascular resistance=selective vasoconstriction->may lead BP to look normal (1st response fight/flight)
Without fluid replacement, hypovolemic (burn) shock will progress
With adequate replacement, cardiac output will stabilize within 24 hours* (dependent on TBSA of burn)
Pulmonary system doe not rebound as quickly- watch for respiratory distress
patho of burns
goal with 48 hours: dump fluid to increase perfusion and MAP to prevent organ failure
24-48 hours into the injury 2 ways: systemic (vasodilation/constriction can move fluid) AND
Diagnosis: fiberoptic -bronchoscopy to look for inhaled burn = swelling/edema, eschar, particles, erythema
-Lavage (wash out debris)
-Repeated as necessary to check progression
CO toxicity
S/S: headache, fatigue, N/V, restlessness, dizziness
- Headache, N/V, DOE-> confusion, lethargy, tachypnea-> seizure, coma, changes on ECG-> death
At low levels: asymptomatic
-Asphyxiant->severe anoxia->brain injury
-Treat with 100% high flow O2- so hemoglobin doesn’t have chance to connect with CO and can reduce 1/2 life to 45 mins (1/2 life = 4 hrs)
Measure CO saturation with serial corboxyhemaglobin levels (blood test)- NOT pulse oximetry (unreliable)
Also use ABGs (acid base balance) to see how body is compensating (metabolic alkalosis)
Inhalation injury
S/S: tachypnea, dyspnea, cough, cough up yellow/sudy sputum, hoarseness, scratchy throat
-do bronchoscopy to check for debris, swelling, ulceration, damaged tissue
-Only present in 10% of cases, but accounts for 20-84% burn mortality
Stages:
-Acute pulmonary insufficiency (not enough air) first 36 hours
-Pulmonary edema: 6-72 hrs 5-30% of pts
-Bronchopneumonia: 3-10 days after 15-60% of pts
pulmonary injuries from burns
Most common cause of death in burn patients after the first 7 days
Skin=your barrier against infection
Prevent: abx, hand washing, sterile technique
What are the signs of septic shock? WBC (sirs of infection), fever (infection or immune response), organ failure (LFT, decrease UO, Bun/CR
What if the patient who was burned ALSO has concomitant injuries? ABC*
ABCs take precedence over caring for specific injuries
Look at fractures, bruising, swelling, hemorrhage, and especially, the cervical spine: especially around head/neck r/t concern for airway
-suspect SCI so immobilize
infection and trauma from burns
triage scale for trauma
1) Resuscitative Phase:
1. . Primary survey (baseline safe)
- -Airway (cervical spine)
- -Breathing and ventilation: lung sounds, respirations - 1st do 100% non-rebreather
- -Circulation and hemorrhage control: HR, BP, pulse, cap refill for extremity
- -Disability (neurological deficit): get baseline; pupils, check sensation, strength (= or bilateral)
- -Exposure (remove irritants (rinse), mind temperature)
2. . Secondary survey (Resuscitation)
- Thorough history and medication list (hx of stroke, meds, diabetes* r/t poor wound healing, kidney disease r/t if pt can filtrate stuff, heart failure r/t dumping fluid)
- -check electrolytes, CBC, EKG, ABG r/t acidosis
- Assess level of burns: linen bowder scale to determine fluid resuscitation
- Lab and diagnostic testing
- Cardiac monitoring
- Fluid resuscitation
- NG and/or Foley: help determine CO and GI becomes permeable so early enteral feeds*
nursing management for burns
Resuscitative phase - primary and secondary survey
first address all life threatening things
Lung involvement at systemic level
Protect airway with early ventilation and immobilization
Hemodynamic support: support vs MAP
primarily accomplished through fluid resuscitation
-so might not give a lot to a compromised pt - get info through UO (30-50 mL/hr) - too much, back off r/t random diuresis
Pulmonary Support: leading cause of death in the first 24 hours r/t swelling, inhalation (hot steam -> ulcerations) (after 24 hrs = infection)
-Blocked upper airway = stridor* - treat with resemic epinephrine to heal upper airway obstruction
-to sooth swollen tissue r/t O2 give humidity, high fowlers, cough/DB, intubate to open airway/get good gas exchange
GOALS:
-Improve oxygenation
-Decrease interstitial edema
-Maintain adequate airway
Bronchopneumonia- typically secondary to another septic source (the burn)
-in bronchial tree (absess on it) - can give prophylactic abx
-Hard to treat - fatal
-regular PN sits in alveoli
nm of burns
Resuscitative phase - primary and secondary survey
Goals*:
-Correct F/E imbalances and protein deficits (give albumin)
-Replace and maintain fluid balance
-Prevent excessive edema (hard to) (get baseline especially lung sounds)
-Maintain UOP of 30-50mL/hr
Formulas are used for fluid resuscitation that calculates fluids based on TBSA and the first 24 hours of injury
Why Lactated Ringers? crystolloid not colloids - LR most closely mimics blood plasma so that’s why
-no actual FFP because expensive and all the fluid would leak into the tissues
–2nd 24 hours the leaking will stop
Why not colloids?
What is the risk for over hydration? See in lungs 1st - I/O*, 30-50 mL hr, baseline
What is the best indicator in fluid resuscitation?
What does this put them at risk for?
fluid resuscitation of burns
Resuscitative phase - primary and secondary survey
TEGRITY
