Test 3 - Neuro Flashcards
What are the 3 main things inside the skull?
Brain, blood, and CSF
What is the Monro-Kellie Hypothesis?
An increase in any of the 3 main components can increase ICP because the skull is rigid
Brain herniation and death will result, if not resolved
C-Spine vs. Airway
C-Spine = airway priority (prevent worsening of injury)
Maintain C-Spine immobilization
Primary Brain Damage
Damage from physical force (open or closed injury)
Secondary Brain Damage
Neuro damage after the initial injury (high ICP, hematoma, etc.)
Open Injury
The skull is open or fractured
Closed Injury
The skull is intact
Linear Fracture
Single, clean break (common in kids)
Least likely to be fatal
Comminuted Fracture
Multiple fractures with potential bone depression into brain tissue
Requires emergency surgery
Basilar Skull Fracture: description
A fracture at the base of the skull, extends into anterior, middle, and posterior fossa
What can a Basilar Skull Fracture cause?
May cause a tear into the dura mater, resulting in a CSF leak
Basilar Skull Fracture: Clinical Manifestations
- CSF leak
- Facial Palsy
- Nystagmus (eye twitch)
- Facial numbness
- Deafness
- Battle’s Sign
- Raccoon’s Eyes
- Hemotympanum
What can a CSF leak cause?
- Otorrhea
- Rhinorrhea
How do you confirm that fluid is CSF?
- Halo Sign
- Test for glucose or chloride
What is Battle’s Sign?
Ecchymosis behind the ear (indicates basilar skull fx)
What is Raccoon’s Eyes?
Periorbital edem (indicates basilar skull fx)
What is hemotympanum?
Blood in the ear drum causing inflammation
What does Basilar Fracture increase the risk for?
Meningitis
What are signs of Meningitis?
- Increased Temperature
- Nucchal rigidity
Basilar Skull Fracture: Nursing Care
- Assess cranial nerves for vision, hearing, or smell
- Avoid NG, nasal intubation, or use of foreign objects into nares/ears!
- HOB 30 degrees
- Avoid straining, coughing, blowing nose (increases meningitis risk)
- Administer abx
- Watch for meningitis s/s
- Surgery if CSF leak >1 week
Closed Head Injury Types (3)
- Concussion
- Contusion
- Diffuse axonal injury (DAI)
Concussion: description and cause
- Brain strikes inside of skull, causing damge at the cellular level
- Caused by blunt force to the head
Concussion: S/S
- Dizziness
- Headaches
- Irritability
- Memory loss
- Brief LOC
What are s/s of post concussion syndrome?
- Personality changes
- Irritability
- Headaches
- Memory loss
- Depression
Is Concussion damage visible on a CT scan?
No. It is at the cellular level
Contusion: description
Bruising of the brain at coup or contrecoup
What is “coup”?
Site of injury
What is “contrecoup”?
Opposite of the site of injury
What is Diffuse Axonal Injury (DAI)?
Direct injury to axons (twist and/or tear of axons)
What is the result of DAI?
Coma or severe intellectual damage
Can axons heal?
No. Once they have been twisted and torn, there is not going back.
Minor Head Injury Education
- If sleeping, wake q3-4 hr for first 48hr
- HA, Nausea, Dizziness = normal, at least 24 hrs
- Notify HCP become severe or do not improve
- No sedatives for at least 24 hrs
- Frequent neuro checks
What is Chronic Traumatic Encephalopathy (CTE)?
A progressive, degenerative brain disease caused by repetitive head traume (athletes, veterans, etc.)
What are S/E of CTE?
- Problems with thinking and memory
- Memory loss
- Confusion
- Impaired judgement
- Early, progressive dementia
Brain Laceration Types (3)
- Epidural Hematoma
- Subdural Hematoma
- Intracerebral Hemorrhage
Epidural Hematoma: description and s/s
- Rapid, arterial bleed above the dura
- Lucid interval**
What is a Lucid Interval?
Brief period of lucidity before 2nd LOC
Subdural Hematoma
- Slow, venous bleed between the dura and the brain
* Takes longer to see in geriatrics r/t brain atrophy with age
Intracerebral Hemorrhage
-A bleed inside the brain
Commonly a ruptured aneurysm
What does decorticate mean?
Abnormal stiffness
Glasgow Coma Scale: purpose
To evaluate neuro status in comatose patients
What are the categories assessed with the GCS?
- Eye (4)
- Verbal (5)
- Motor (6)
GCS scores: 15, 7, 3
15- excellent
7- <8 = airway issues, needs intubation
3- completely comatose
Decorticate Positioning: Indicates
Lesion in the cortiocspinal pathway
Decerebrate Positioning: Indicates
Lesion in the brainstem
Normal ICP Value
5-15 mmHg
What ICP value indicateds intracranial HTN?
> 20 mmHg
Measurement of ICP
- HOB at 20-30 degrees
- Level transducer with foramen of Monro/ “Tragus” (the ear)
What is the relationship between ICP and CPP?
Increased ICP = decreased CPP
What can too elevated CPP cause?
Rupture of brain blood vessels
Normal CPP Value
60 mmHg (max 80 mmHg)
How does BP (MAP) relate to CPP?
BP needs to be in a healthy range to maintain proper CPP
How do you calculate MAP?
[(2 x Diastolic BP) + Systolic BP]/3 = MAP
How do you calculate CPP?
MAP - ICP = CPP
What are clinical manifestations of increased ICP?
-#1 sign = LOC change
-Pupillary changes (ipsilateral/same side as injury)
Bilateral changes indicates worsening
-Papilledema
-Motor Changes
-Headache
-Projectile Vomiting
-Cushing’s Triad
What are the steps in worsening motor changes?
Decorticae, Decerebrate, Flaccid paralysis
What is Cushing’s Triad?
- HTN with widdening pulse pressure
- Bradycardia
- Alternating respiratory patterns (Cheyne Stoke)
What are Cheyne Stoke Respirations?
Segments of tachypnea followed by apnea
Maximum Na Level
160
Medicinal Care to reduce Cerebral Edema
-Hypertonic saline (3% NaCl)
-Osmitrol (Mannitol)
Use a filter* (d/t crystallization)
Bolus for best results
-Dexamethasone (Decadron), Solumedrol = steroids per protocol
-Avoid hypotonic fluids (such as D5W or 1/2 NS) will worsen condition
Normal Osmolality Value
295 - 320
What type of medications do you use to treat Vasogenic Edema?
Diuretics
What type of medications do you use to treat Cytotoxic Edema?
Steroids
What is Vasogenic Edema?
Fluid accummulation outside of cells; damage occurs to BBB
What is Cytotoxic Edema?
Fluid accummulation inside of cells
What is the affect of Hypertonic Solutions?
Pulls fluid out of cells, shrinking them
Non-Pharmalogical Care for increased ICP/Cerebral Edema
-HOB degrees to improve venous drainage from brain
-Keep Blood Glucose WNL
Monitor q4h
Normal BG Value
80-120 mg/dL
Significane of hyperglycemia in brain injury
Predictor of poor outcome - associated with UTI, pneumonia, etc.
BP control with increased ICP
- When HTN is severe (>180/95 mmHg)
- Avoid hypotension = cerebral ischemia
What is a severe HTN value?
> 180/95 mmHg
Why do you need to avoid hyperventilation?
hyperventilation = low CO2 = vasoconstriction = ischemia
End tidal CO2 value
30-35 mmHg
PCO2 (ABG) Value for Brain Injury
35-38 mmHg
What can cause a seizure?
Too high temperature
Room Set up for Brain Injury
-Patient’s Temperature is kept ~97 F (36 C)
Need to slowly lower body temp to avoid shivering
-Bedside swallow studies PRN
-Decrease stimuli
-Avoid clustering of care
Measures to prevent ICP increases
What kind of sedatives are given for brain injury?
Non-Barbituates (Diprovan [Propofol])
Anticonvulsants (within 1 weeks of injury)
S/E: bradycardia, hypotension
“Keppra” (1000 mg)
What does OT do?
Helps people regain ability to do ADLs
Brain Death: description
Non-reversible brain injury that precedes cardiac arrest
Organ donation requirements
Donor must have intact heartbeat and circulation (MAP >60)
Organ Donor Eligibility
<65 years old with:
No hx of metastatic cancer
No active sepsis
No evidence of communicable diseases such as Hepatitis or HIV/AIDS
Brain Death Determination
Must be “warm and dead”
- Normal temperature
- No brain activity depressing drugs
- SBP >100
- Etiology of coma known
- No brainstem reflexes (pupillary, ocular, corneal, gag, and cough)
- Apnea test
What is an Apnea Test?
Don’t extubate, but disconnect from the ventilator and only give O2
Compare ABG b4/after for exponentially increased CO2
Additional Brain Death confirmatory tests
- Cerebral angiogram
- Electroencephalography (EEG)
- Transcranial doppler
What is seen on a Cerebral Angiogram in brain death?
Decreased bloodflow (“Hollow skull”)
Nurse’s Role in Brain Death Care
- Follow state/facility procedures
- Don’t use misleading terms (i.e life support)
- Don’t perform misleading actions (overly cheery, talking to patient as if conscious)
- Document accurate Time of Death
What are things that cause increased Serum Osmolality?
- Dehydration
- Lasix
- Diuretics: Mannitol
- Hypertonic Fluids
What is the function of the Spinal Cord?
It is the highway between the CNS and the Brain
What do the Spincal Cord’s Upper Neurons do?
Send signals from the brain to the spinal cord
What do the Spinal Cord’s Lower Neurons do?
- Sensory: send signals from spinal cord to the brain
- Motor: send signals from spinal cord to the body (reflexes, muscles, etc.)
How many of each Spinal Nerve?
Breakfast, Lunch, Dinner
Cervical - 8
Thoracic - 12
Lumbar/Sacral - 5 each
SCI Mechanisms of Injury
Hyper Flexion
-head on collision
Hyper Extension
-rear end collision
Axial loading
-compression injury
Rotational
-head turned beyond normal range
Penetrating Injury
-bullet, stab, etc.
What area of the spine are most commonly injured?
- Cervical
- Thoracolumbar
(Areas with the most mobility)
What impacts SCI outcomes?
Severity and level of injury
Higher injury = Higher disability
Complete (permanent loss of function below LOI) or Incomplete
What is Brown Sequard?
Ipsilateral (same as injury side): loss of motor function, sensation, vibration affected
Contralateral: loss of pain/temperature affected
Brown Sequard: Affected Side
No motor function, full sensation
Brown Sequard: Unaffected Side
No sensation, full motor function
Spinal Shock: onset and duration
Immediate onset after injury
Temporary (lasts 4-6 weeks)
Spinal Shock: S/S
- Complete loss of motor function, including Bowel and Bladder (flaccid paralysis)
- Gradual return of function
- Positive anal wink (assesses S5 Nerve, which is lower than the nerves for toes)
- Loss of sensory function
Spinal Shock: Care
- NPO = NGT need
- Foley Catheter needed
Neurogenic Shock: onset
Immediately after injury
Neurogenic Shock: S/S
Only shock with bradycarida and hypotension***
Temp SNS loss = PNS taking over
PNS activation = decreased HR and vasodilation
BP and heart rate drop
Flushed, warm, dry skin
Neurogenic Shock: Interventions
- Vasopressors
- Dopamine
- Volume Replacement
- Ace Wrap
Autonomic Dysreflexia: onset and cause
Delayed = a few weeks post-injury
Any nerve over stimulation (especially bowel and bladder)
Autonomic Dysreflexia: S/S
- HA, flushing, warmth
- HTN (d/t vasoconstriction) = SBP 20-40+ baseline
- Bradycardia
- Anxiety
- Cold skin below LOI
What does a LOI above T6 cause?
Loss of SNS
Autonomic Dysreflexia: Interventions
- Elevate HOB
- Remove stimulus
- VS q2-5 minutes
- If BP remains elevated, IV meds
Autonomic Dysreflexia: Pathology
Nerves don’t communicate
SNS is triggered below LOI
PNS is triggered above LOI
Autonomic Dysreflexia: above LOI
PNS triggered
- HA
- Flushed
- Vasodilation
Autonomic Dysreflexia: below LOI
SNS triggered
- Cold
- Clammy
- HTN
Where is T4?
Nipple line
Where is T10?
Belly button
Autonomic Dysreflexia: Goals and Teaching
Goal: prevent episodes from occurring
Teaching:
- recognize triggers (Bowel and Bladder = top 2)
- Remove stimulus quickly
- Maintain effective bowel and bladder regimens
Bladder Regimen
-Straight Cath (sterile techiniqure) after voiding Use BR q2h after meals -Bladder scans to check residuals -DC regimen if residual urine <100 mL -Increase fluids 2,000 to 2,500 mL/day -S/S UTI
UTI: S/S for sensory impaired
Urine odor and appearance
Stimulating Bladder
- Valsalva
- Tighten abs
- Straight cath
- Stroke inner thigh
- Pull pubs
DC if residuals <100 mL
Bowel Regimen
- Maintain routine
- High fiber and fluid if allowed
- Rectal stimulation
- Mini Enema
- Manual decompaction
SCI reproductive effects
Men may have problems with erection, ejaculation, or both
Women can conceive and get pregnant
Transient Ischemic Attack (TIA)
Transient focal neurologic dysfunction w/o acute infarction
Mini-stroke - “warning sign” of full stroke potential
1/3 of pt. within a year
S/S resolve in about 60 min
Stroke: Risk Factors
- > 60 yr
- African America
- Female
- HTN
- High cholesterol
- Diabetes
- Lifestyle factors
- A. Fib d/t clotting at appendage of heart
Stroke: Types
Ischemic (MOST COMMON)
-Clots, thrombus, or embolus
Hemorrhagic
-broken blood vessel
Stroke: Assessment
GFAST
G.F.A.S.T
G- gaze F- facial droop A- arm weakness S- speech difficulty T- time to call for help
What is the time limit for thrombolytic treatment of strokes?
4.5 hours maximum
What is the time limit for mechanical removal of clots in strokes?
24 hrs
What are the best diagnostic tests for stroke?
- # 1 = urgent CT, no contrast
- MRI
- Fingerstick BG (to see if BG level is cause)
- O2 saturation
- 12 lead ECG
- CBC
Stroke: S/S
Based on:
- Location
- Size
- Perfusion
- Collateral blood flow
Where are the most common strokes?
Middle Cerebral Artery
Basilar Artery Syndrome: S/S
Affects the brainstem; 95% fatal
- Dizziness
- Ataxia
- Tinnitus
- Nausea/Vomiting
- One sided weakness
Test function: touch nose, touch RN finger
Right MCA
Largest cerebral artery; most affected by stroke
- Left* sided weakness
- Eyes turned toward* stroke (right)
- Left side neglect
- Disorientation, impulsive, poor judgement, constant smiling, lack of position sensing
Left MCA
- Right* sided weakness
- Altered intellectuality, slow, cautious, anxious, depressed, dyslexia or alexia
- No hearing deficit
- Eyes turn towards stroke
Left MCA: Aphasia
Expressive: ask “what is this object?”
Receptive: tell “give me a thumbs up”
Left MCA: Dysarthia
Loss of speech
Expressive Aphasia: area and lobe
Broca’s Area
Frontal lobe
-Difficulty in expressing thoughts (written or verbal)
Receptive Aphasia: area and lobe
Wernicke’s Area
Temporarl lobe
- Unable to understand (written or vebal)
- Neologisms
Global/Mixed Aphasia
Combination of Expressive and Receptive Aphasia
Stroke: Motor changes
- Hemiplegia/Hemiparesis (one side paralysis)
- Motor changes on opposite* side of stroke location
Stroke: Sensory changes
- Agnosia: can’t recognize familiar objects
- Apraxia: inability to carry out skilled movements that were previously known
- Visual Fields Deficit: hoomonymous hemianopsia “field cut”
Major problem with Cranial Nerve deficits
Aspiration pneumonia
Cranial Nerve Deficits
-Impaired swallowing
Test: give 1 tsp of water, fails if wet/gurgling voice
Fail = NPO, IV meds, suppository not PO meds
Implications for clear oral test
- Sitting straight up
- Soft/semisoft foods
- “Thick it”
- Fodd supplements
- Daily weight
- I&O
Impaired Communication: Care
- Speech therapy
- Facial muscle exercises
- Face client when speaking
- Anticipate needs
Impaired Communication: Nursing Considerations
- Speak slowly, not loudly
- Divide tasks into smaller units
- One step commands
- Anticipate needs
- Picture boards (Boca’s area)
- Avoid yes/no questions
- Use understandable vocabularies (Wernicke’s area)
Stroke: Medical/Surgical Interventions
-CEA (if plaque >70&)
-Craniotomy to evacuate clot to prevent ICP increase
-BP
Hemorrhagic stroke (keep close to 140 SBP, but not over)
Ischemic stroke (Keep BP less than 185/110)
-Stent retreivers
Stroke: Drug Therapy
-Fibrinolytic/Thrombolytic therapy
T-PA
Alteplaze (activase)
Max dose: 82 mg, flush at rate of admin
Stroke: Drug Therapy - Criteria before T-PA administration
-No acute hemmorrhage
-Tx 4.5 hr or less from onset of S/S
-BP less than 185/110
Anti-HTN meds
-Neuro and VS assessment: before and after infusion (q15min)
Stroke: Anti-HTN Meds
Labetalol: 10-20 mg IV over 1-2 minutes
Nicardipine: 5 mg/hr IV
Fibrinolytics/Thrombolytics Exclusion Criteria
- Significant head trauma, intraspinal surgery, or stroke in past 3 months
- Active internal bleeds
- Bleed predisposition (plt <100,000, INR >1.7, high PTT)
- Severe uncontrolled HTN
What meds can be taken with Fibrinolytics?
- Aspirin
- Plavix
How is treatment window determined if pt. wakes up with S/S of stroke?
Based on “last known well”
Post Activase/Altepase: Nursing Care
- Coag studies
- Neurochecks (often)
- Bed rest
- IV access maintained from before tx
- No ASA, etc. for 24 hr
Ant-Coags for CVA
Heparin PTT 1.5-2.5x baseline (baseline = 20-30 sec) Warfarin (Coumadin) PT/INR INR: 2-3 If cardiac origin, INR 3-4 Antidote: Aquamephyton (Vitmain K) Kcentra (for URGENT Coumadin reversal)
Newer Drugs for CVA
“-xaban”
Lovenox (Enoxaparin)
Antiplatelets
-ASA (325 mg)
-Plavix (Clopidogrel)
Cerebral Aneurysm: Definition
An out-pouching or dilation of a cerebral artery
Cerebral Aneurysm: Most Common Site
Bifurcation of blood vessels in the Circle of Willis
Cerebral Aneurysm: Etiology
- HTN
- Atherosclerotic plaque build up
- Infectious aneurysm
- Congenital defect
e. g. Arteriocenous malformation (AVM)
Cerebral Aneurysm: Types
- Berry: most common
- Fusiform (saccular): dilated vessel wall, out-pouching
- Mycotic: rare
Cerebral Aneurysm: S/S
Before rupture- asymptomatic
After rupture:
- Thunderclap headache (worst headache of life)
- Pain above and behind the eye
- Dilated pupil
- Photophobia*
- Seizure, motor deficit
- Nucchal rigidity*, irritability, blurred vision, positive Kernig’s and Brudzinki’s Signs
- Unconscious
If not treated successfully -> death
Brudzinki’s Sign
As the neck is flexed, pain causes the knees to flex in order to reduce the pain
Kernig’s Sign
Hips and knees flexed and straigtened = pain in hamstring
Cerebral Aneurysm: Diagnosing
- CT
- Arteriogram
- MRI
If results, unclear -> lumbar puncture (look for blood)
Cerebral Aneurysm: interventions/precautions
- Bed rest
- BP kept within parameters
- Dark/Quiet environment
- Limit external stimuli (to present ICP increase)
- Avoid vagal stimulation
- Monitor/manage pain and stress
- TEDs or SCDs
- Surgery
Aneurysm Surgical Interventions
Clip placement, Vessel wrapping, or Coils
AVM Interventions
Embolization or Radiosurgery
-To decrease the number of feeding arteries to aneurysm
Aneurysm Responsibilities: Post-op
-Monitor neuro status
-Maintain BP and CPP
-Monitor for re-bleed
Peak incidence: 24-48 hrs
-Monitor for hyponatremia (can cause cerebral edema)
-Monitor for hydrocephalus (due to CSF clogging)
Vasospasm: Nursing Responsibilities
-Monitor for S/S (altered LOC -> assess with GCS)
Occurs between day 4-14 post op
-Diagnostic: transcranial doppler**
-Hemodynamic augmentation
Vasopressors (dopamine and Nor-Epi***)
Vasospasm: preventative med
Nimodipine (s/e Hypotension)
-Not all CA Channel Blockers*
Brain Tumors: Primary
Originate in the CNS and rarely metastisize
Brain Tumors: Secondary
Results from metastasis from elsewhere
Brain Tumor: Classifications
Histology: Malignant or Benign
Location: Supra- or Infra-tentorial
Brain Tumor: Types
Malignant:
- Glioblastoma (worst)
- Astrocytoma
Benign: -Meningiomas -Pituitary tumors -Acoustic neuromas S/S: tinnitus, hearing loss, dizziness, and vertigo
Brain Tumor effects (regardless of location)
- Cerebral edema
- Brain dysfunction
- Increased ICP
Brain Tumor: Manifestations
- Headache (worse in am)
- Vomiting (d/t vomit center stimulation)
- Personality changes
- Aphasia
- Ataxia
Brain Tumor: Complications
-Increased ICP
-Bleeding
-Cerebral edema
Vasogenic: BBB disrupted
-Seizures
-Venous thromboembolism
Brain Tumor: Diagnosis
- CT scan or MRI
- Cerebral angiography
- Chest X Ray
- Tissue Biopsy
Brain Tumor: Post op Care
-Monitor neuro deficit
-Avoid activities that increase ICP
No bending, lifting, straining, and Valsalva maneuver
-Monitor s/s infection, wound care, drainage care
-NPO for 24hrs to avoid potential aspiration pneumonia
-Monitor CBC, e-lytes, and osmolarity
-Emotional support
Brain Tumor: Post op Positioning
Supratentorial
- HOB 30 degrees
- Head, neck neutral position
- May turn to side
- Avoid placing on op side if large tumor
Infratentorial
- Flat
- Side lying
Brain Tumor: Post op Care
- Pituitary tumor removal
- Monitor DI or SIADH
- I&O
- DI -> increase serum osmo, UOP, hypernatremia*
- SIADH -> hyponatremia*
Brain Tumor: Post op Care - DI
- Administer synthetic ADH
- Daily weight
- Oral intake to balance output
Brain Tumor: Post op Care - SIADH
- Fluid restriction
- 3% NaCl solution for severe hyponatremia
Seizures
Abnormal electrical activities
Seizures: S/S
Changes in:
- consciousness
- Motor
- Sensory
- Behavior
Seizures: Patho
Primary: idiopathic
Secondary (non-epileptic): trauma, surgery, tumor, stroke, infection, substance abuse, low O2
Epilepsy:
2 or more unprovoked seizures, 24 hrs apart
Low GABA
What is the function of GABA?
GABA is an inhibitory neurotransmitter
Absence of Seizures
- Brief LOC
- Blank stare, daydreaming
- Unresponsive
- Minimal to no muscle alt.
- Hand movement, lip smacking, swallowing
Aura in advance of seizure
Lamotrigine (Lamictal) - Risk
Stevens-Johnson Syndrome (life threatening rash)
Carbamazepine (Tegretol) - Risks
SIADH
Stevens-Johnson Syndrome (Asian HLA-B carriers)
Valproex (Depakote) - Risk
Teratogenic
Teach patients and check HCG levels
Benzodiazepines: Timing and Names
Within 6 minutes to prevent status epilepticus
Diazepam (Valium)
Clonazepam (Klonopin)
Phenobarbital (Luminal)
Levetiracetam (Keppra) vs. Phenytoin (Dilantin)
Keppra is safer
Phenytoin (Dilantin): Risk
Hepatoxicity risk:
- Increased ALT
- Increased AST
- Jaundice
Dilantin Blood Levels
Normal: 10-20
Toxic: >30
S/E: GI, anemia, gingival hyperplasia
Status Epilepticus
- Seizures lasting longer than 5 minutes
- Two or more seizures without full recovery of consciousness between
Seizures >30 = neuro complications
Status Epilepticus: etiology
Trauma, drug/alcohol withdrawal
Status Epilepticus: actions
-ABC
-Safety (bed low, rails x4, etc.)
-Call a rapid response
-IV Benzos ( Ativan, Valium, Versed)
-Keppra
-NPO
-Post Ictal (seizure) Care
ABC, safety, prevent aspiration
Seizure Precautions
- O2 and suction equipment nearby
- Saline locked IV access
- Side rails up x4 (no padding)
- Bed low
- No tongue blade
Seizure/Epilepsy: Education
-Anti Epileptic drugs can’t be stopped, even if seizures stop
Driving? - most states = clear of seizures for 6 months
Meningitis: definition
Infection of the meninges that surround the brain and spinal cord
Meningitis: cause
Primary: Viral/Aseptic, fungal, or bacterial
Secondary: following surgery or trauma
Where do Meningitis outbreaks happen?
Areas of high population density
Who is most likely to get Meningitis?
Young (<5), old, or immunocompromised
Bacterial vs. Viral Meningitis: severity
Bacterial is much more lethal
Viral is self-limiting
Meningitis: S/S
- Meningismus (Meningeal irritation)
- Divergent degrees of neuro changes
- HA
- N/V, fever, chills, generalized aches and pains
- Tachycardia
-Red macular skin rash
Meningismus: S/S
- Photophobia
- Nuchal rigidity
- Positive Brudzinski’s or Kernig’s signs (some pts. don’t have these)
What other condition has similar S/S of meningitis?
Aneurysm
Meningitis: Diagnostics
- CT (check for aneurysm)
- CBC, CMP
-Lumbar puncture and CSF analysis to confirm
Kernig’s Sign
Move legs, bending knees = hamstring pain
Brudzinski’s Sign
Tilt head to chest = knees raise to reduce pain
CSF Analysis: Bacterial vs. Viral Meningitis
Bacterial: cloudy CSF, decreased Glucose
Viral: clear CSF, normal glucose
Meningococcal meningitis: precautions
Droplet and standard:
- Mask when <3 feet of pt
- Gloves to touch body fluids
- Door can be open
-Pt. mask if outside room
PPE: donning order
- Gown
- Mask
- Goggles/face shield
- Gloves
PPE: doffing order
- Gloves
- Goggles/face shield
- Gown
- Mask
Bacterial Meningitis: Prevention
- Vaccination
- Prophylactic abx within 7 days of exposure
What is the only stroke med?
T-PA
Transient Ischemic Attack (TIA): teaching
- Diet
- Exercise
- ASA: 325 mg dose
- Plavix (clopidogrel)
Penumbra
The area that remains viable after stroke w/ rapid intervention
Anti-platelet use: before/after T-PA admin
Before: not a problem
After: not for 24 hrs
Hemorrhagic Stroke: BP goal
140 SBP
Ischemic Stroke: BP goal
185/110
T-PA contraindicated meds
“-xaban” within 24 hrs
ABG values for TBI
pH: 7.35 - 7.45
CO2: 35 - 38
HCO3: 22 - 26
Meds to decrease ICP
Mannitol
3% NaCl (hypertonic fluid)
Steroids (Increases BG and GI bleed risk)
ICP: value
5 - 15
CPP: value
> 60
TIA aspirin dose
325 mg
What needs to be looked out for 4-14 days post-op?
Vasospasms d/t increased risk