Neuro week 2 Flashcards
Coma
Unarousable unresponsiveness, no purposeful responses to internal or external stimuli
Akinetic mutism
state of unresponsiveness to the environment in which the patient makes no voluntary movement
persistent vegitative state
unresponsive patient resumes sleep-wake cycles after coma but is devoid of cognitive or affective mental function
minimally conscious state
inconsistent but reproducible signs of awareness
Locked-in syndrome
lesion affecting the pons and results in paralysis and the inability to speak, but vertical eye movements and lid evaluation remain intact and are used to indicate responsiveness
Clinical manifestations for altered level of consciousness
Occur along a continuum, and the clinical manifestations depend on where the patient is on the continuum.
Initial alterations = subtle behavioral changes, such as restlessness or increased anxiety. The pupils, normally round and quickly reactive to light, become sluggish (response is slower)
As the patient’s state of alertness and consciousness decreases, changes occur in the pupillary response, eye opening response, verbal response, and motor response.
As the patient becomes comatose, the pupils become fixed (no response to light). The patient in a coma does not open the eyes to voice or command, respond verbally, or move the extremities in response to a request to do so
Altered level of consciousness: assessment
evaluation of mental status, cranial nerve function, cerebellar function (balance, coordination), reflexes, and motor/sensory function
Altered level of consciousness: diagnostics
GCS CT Perfusion CT MRI MRS EEG PET SPECT
Altered level of consciousness: labs
BG electrolytes serum ammonia Liver function tests BUN serum osmolality prothrombin partial thromboplastin etc
Altered level of consciousness: medical management
nutritional support, adequate O2 and perfusion, circulation
Go review and take notes on slide 4 “protecting the patient”
you may already know a lot of these things that is why i am not putting it in here
Head injury: focus
prevention (seatbelt, helmet, etc.)
Primary head injury
Initial damage (concussion, contusion, laceration, torn blood vessel)
Secondary head injury
Ensuing hours or days after the injury, resulting in cerebral edema, ischemia, seizures, infection, hyperthermia, hypovolemia, hypoxia
Skull fractures: simple, comminuted, depressed, basilar
simple: break in continuity
Comminuted: more than 2 pieces
Depressed: compressed onto brain tissue
Basilar: back of head area
What does a patient with a skull fracture generally look like?
Depends on severity. Confused, forgetful, not as sharp as they used to be.
What do skull fractures frequently produce?
Hemorrhage from the nose, pharynx, or ears, and blood may appear under the conjunctiva. You may also note an area of ecchymosis that may be seen over the mastoid (Battle sign) develop 12-24 hours after injury.
When might a basilar skull fracture be suspected?
suspected when cerebrospinal fluid (CSF) escapes from the ears (CSF otorrhea) and the nose (CSF rhinorrhea). A halo sign (a blood stain surrounded by a yellowish stain) may be seen on bed linens or on the headdressing and is highly suggestive of a CSF leak
Why is drainage of CSF a serious issue
meningeal infection, abscess formation, and osteomyelitis can occur if organisms gain access to the cranial contents via the nose, ear, or sinus through a tear in the dura
Skull fracture: assessment
close observation, do not blow nose
Skull fracture: something the nurse should remember to do
keep HOB at 30 or above to reduce ICP and promote spontaneous close of the leak
Concussion
(also referred to as a mild TBI) involves an alteration in mental status that results from trauma and may or may not involve loss of consciousness.
Concussion: how long does it last and what are the s/s
no longer than 24 hours and may include symptoms such asheadache, nausea, vomiting, photophobia (sensitivity to light), amnesia, and blurry vision
Concussion: treatment
observing the patient for symptoms, including headache, dizziness, lethargy, irritability, anxiety, photophobia, phonophobia (fear of sound or of speaking aloud), difficulty concentrating, and memory difficulties.
The occurrence of these symptoms after the injury is referred to aspostconcussive syndrome
Contussion
more severe than concussion; bruising of brain with possible surface hemorrhage
Contussion: s/s
patient unconscious for more than few seconds or minutes
– may lie motionless, faint pulse, shallow respirations, cool, pale skin
– may be aroused with effort but soon slips back into unconsciousness
Diffuse axonal injury
widespread damage to axons in the cerebral hemispheres, corpus callosum, and brainstem. It can be seen with mild, moderate, or severe head trauma.
Diffuse axonal injury: s/s
- The patient experiencesimmediate coma, global cerebral edema, decorticate and decerebrate rigidity, orposturing
Decoricate
posturing involves abnormal flexion of the upper extremities and extension of the lower extremities and indicates damage to the upper midbrain;
Decerebrate
posturing involves extreme extension of the upper and lower extremities and indicates severe damage to the brain at the lower midbrain and upper pons
Intracranial hemorrhage: Epidural hematoma
symptoms are caused by expanding hematoma
Momentary loss of consciousness then will become lucid – CSF trying to compensate and regain hemostatsis.
If not – sudden signs of compression appear – deteriorates rapidly. EXTREME emergency – burr holes to decrease pressure
Intracranial hemorrhage: Subdural hematoma
Collection of blood between dura and brain
a. acute (24-48)
b. subacute (48 hours-2 weeks after injury)
change in LOC, pupils reaction, hemiparesis, gait disturbances, headache, aphasia, AMS, agitation
Intracerebral hemorrhage: solution
decompressed caniotomies
Brain injury management
A patient with a head injury is presumed to have a cervical spine injury until such injury is ruled out; therefore, immobilization of the spine via cervical collar, spinal backboard, and the avoidance of movement is essential.
TBI focused assessment
a. ALOC
b. Pupillary abnormalities
c. Sudden onset neuro deficits
d. changes in vitals
e. changes in vision, hearing and sensory functions
f. headaches
g. seizures
Treatments to prevent secondary brain injury
stabilization of CV and respiratory function to maintain adequate cerebral perfusion, control of hemorrhage and hypovolemia, and maintenance of optimal ABG
ICP: Monro-Kellie hypothesis
because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others. Due to this limited space, the brain compensates by moving around CFS, increase the absorption or decreasing its production, or decreasing blood volume. If these compensations were not made, ICP would rise
Normal ICP
5 - 15
When does treatment to correct ICP begin
treatment begins at 20
Early signs of increased ICP
HA, N/V, behavior change (restless, disorientation)
Change in LOC.
Agitation
Slowing of speech
Delay in response to verbal orders
Any sudden condition such as restlessness, confusion, increased drowsiness has neurological significance.
How might you assess someone if you were worried about increased ICP?
GCS, sternal rub, nail bed stimulation
increased ICP: priority intervention
airway, restoring neuro function, HOB 30 or more, fluid restriction
increased ICP: medications used/not used
Used: Mannitol, hypertonic solutions
NO: hypotonic solutions (0.45% NS)
increased ICP: assessment
Lumbar puncture is avoided in patients with increased ICP, because the sudden release of pressure in the lumbar area can cause the brain to herniate
Late signs of increased ICP
Comatose
Decreased rr and pulse
Increased temp., BP, and pulse pressure
Fluctuating pulse
Management of ICP
Osmotic diuretics Fluid restriction Draining CSF Control fever Maintain systemic BP and oxygenation Reduce metabolic demands HOB 30+ Neck stays aligned
How can a nurse reduce metabolic demands?
dim lights, decrease stimulation, bed rest, anxiolytics, cluster cares
What is the primary hormone with the posterior pituitary gland?
ADH (vasopressin) –> think fluid balance with this hormone
HYPO-ADH =
diabetes insipidus (HIGH AND DRY)
Hypo-AHD (diabetes insipidus): manifestations
peeing weak, thready pulse decrease skin turgor dizzy, low BP hemoconcentration - hypernatremia
Hypo-ADH (diabetes insipidus): treatment
Need to replace vasopressin using desmopressin
Thiazide diuretic to help stimulate vasopressin
DO NOT RESTRICT FLUID
Hyper-ADH =
SIADH (too much ADH)
Hyper-ADH (SIADH): manifestations
Reabsorbing more water Bounding pulse Increase BP HA Edema USG - 1.030 (dark, concentrated) Hemodilution - severe hyponatremia
Hyper-ADH (SIADH): tx
I&O Daily weight cognition HOB flat to promote venous return Fl. restriction Furosemide only is Na is > 125
What is an indication that lasix should NOT be given
Na+ less than 125
Intracranial surgery: craniotomy
involves opening the skull surgically to gain access to intracranial structures
Bone flat
– remove portion of skull; allows brain to swell
Burr hole
drill into brain to relieve presssure
Types of intracranial surgery
Supratentorial
Infratentorial
Transsphenoidal
Nursing interventions: Supratentorial
Maintain head of bed elevated at 30 degrees, with neck in neutral alignment
Nursing interventions: Infratentorial
Maintain neck in straight alignment
Avoid flexion of the neck to prevent possible tearing of the suture line.
Nursing interventions: Transsphenoidal
Maintain nasal packing in place and reinforce as needed.
Instruct patient to avoid blowing the nose.
Provide oral care according to institutional procedure.
Keep HOB elevated to promote venous drainage
What are possible complications of manipulation of the pituitary gland that you might see with a transsphenoidal intracranial surgery
CSF leak, visual disturbances, post op meningitis, SIADH
Intracranial surgery: postop nursing management
Reducing cerebral edema (dexamethasone)
Pain relief
Prevent sz. (phenytoin, levetiracetam)
Monitor ICP
Complete spinal cord lesion
total loss of sensation and voluntary muscle control below the lesion
What are the most common spinal cord injuries?
C5 & 6
T12
L1
Primary vs secondary spinal cord injuries
Primary: result of initial trauma
Secondary: can be reverses during 4-6 hours after. Results from nerve fibers swell and disintegrate leading to hypoxia, ischemia, edema, hemorrhage
What are we concerned about the higher the spinal cord injury?
respirations
Acute complications SCI: spinal shock
Depression of reflex activity in spinal cord below the level of injury
What may be affected with spinal shock, and how is this treated?
bowel and bladder reflexes may be impacted, which can cause bowel distention and paralytic ileus. This is treated with NG tube to decompress the intestine.
Acute complication of SCI: neurogenic shock
Loss of ANS below level of lesion
Neurogenic shock manifestations
Vital organs are impacted, leading to hypotension, bradycardia, decreased cardiac output, venous pooling in extremities, peripheral vasodilation, warm skin.
Patient does not perspire on the paralyzed portions of the body (close observation for early detection of fever)
Acute complication of SPI: DVT
Related to immobility
- measure thigh and calf daily
- anticoagulation when brain injury and other bleeding have been ruled out
Acute complication of SCI: orthostatic hypotension
First 2 weeks following SCI - unstable and low BP due to loss of reflex vasoconstriction
- lesions above T7
- slow position changes
- compression stockings and abdominal binders all times
SCI Emergency Management: ASIA Impairment scale
go look at this slide 22
Autonomic Dysreflexia
Medical emergency – exaggerated autonomic response to stimuli that are harmless in normal people.
When might autonomic dysreflexia manifest, and how does it manifest?
Occurs after spinal shock has resolved with injuries above T6. HA Paroxysmal hypertension Profuse diaphoresis Nausea Nasal congestion Bradycardia
What can trigger autonomic dysreflexia?
distended bladder
constipation
stimulation of the skin
Autonomic dysreflexia: interventions
HOB raised Bladder mt Constipation assessed Skin assessed Hydralazine IV
What is a seizure
episodes of abnormal motor, sensory, autonomic, or psychic activity (or a combination of these) that result from sudden excessive discharge from cerebral neurons
What is the active phase of a seizure called
Ictal
Status epilepticus
Someone who can not stop seizing
What are 3 things needed for a seizure?
- Excitable neurons
- increase in excitatory glutaminergic activity through recurrent connections to spread the discharge
- Reduction in activity of normal inhibitory GABA projection
Causes of seizures
Cerebrovascular disease Hypoxemia of any cause, including vascular insufficiency Fever (childhood) Head injury Hypertension CNS infections Metabolic and toxic conditions (e.g., kidney injury, hyponatremia, hypocalcemia, hypoglycemia, pesticide exposure) Brain tumor Drug and alcohol withdrawal Allergies
Focal seizure
Partial seizure
With or without consciousness
In one spot of brain
May not even notice them
Generalized seizure: Tonic-clonic
Generalized seizures that affect the entire brain; they begin with rigidity (tonic phase), followed by repetitive clonic activity of all extremities characterized by stiffening or jerking of the body.
tonic seizures
characterized by muscle stiffening, dilation of the pupils, and altered respiratory patterns; the body becomes stiff and the person may fall backward. The seizure usually lasts less than 1 minute, and recovery is rapid.
Clonic seizure
Characterized by jerking movements, which involve muscles on both sides of the body
Absence seizures
Short episodes of staring and loss of awareness
Atonic seizures
Sudden loss of muscle tone, resulting in falls or a “drop” to the ground, with rapid recovery
Myoclonic seizures
Characterized by jerking (myoclonic) movements of a muscle or muscle group, without loss of consciousness
What are the types of epilepsy?
Focal and generalized
Focal seizure - retains awareness
There is no impairment of consciousness, similar to simple partial seizures, may have movement of body parts, may experience an aura.
Focal seizures - altered awareness
There is impairment of consciousness, similar to complex partial seizures, this can spread to both hemispheres of brain.
Where in the brain is a generalized seizure happening
both hemispheres
What are the types of generalized seizures
Tonic-clonic Tonic Clonic Absence Atonic Myoclonic
What is important to keep in mind with someone who has received long-term anticonvulsant therapy
These patients are at increased risk for fractures resulting from bone disease (osteoporosis, osteomalacia, and hyperparathyroidism), which is a side effect of therapy.
so…
During seizure, the patient is protected from injury with sz. precautions and monitored closely.
What test will be performed of someone having sz or someone suspected of having sz?
EEG - electrodes on head
What is important information to gather of someone who is experiencing sz?
Hx. clot, stroke, medication, stress, alcohol use, withdrawal, last alcoholic drink, blood thinners, etc.
If you know someone is being admitted for sz., how will you prepare the room?
Privacy provided as soon as possible Loose clothing 2 or 3 side rails up Bed lowest position Bed rails padded Pillow under head O2 tubing O2 and suction available
Keppra (Levetiracetam): what?
anticonvulsant
Keppra (Levetiracetam): dose-related sfx
Somnolence, dizzy, fatigue
Keppra (Levetiracetam): toxic effects
unknown
Seizures: gero considerations
Increased incidence
Treat underlying cause
Absorption, distribution, metabolism and excretion of medications are altered in the older adult as a result of age-related changes in renal and liver function
Why might there be an increased incidence of seizures among the gero population
medication, head injury, dementia, infection, alcoholism, and aging
Triggers for migraine
Foods that contain tyramine, such as chocolate, cheese, coffee, dairy products
Dietary habits that result in long periods between meals
Menstruation and ovulation (caused by hormone fluctuation)
Alcohol (causes vasodilation of blood vessels)
Fatigue and fluctuations in sleep patterns
Migraine headaches: teaching
Headache diary
Stress management and lifestyle changes
Correct pharm management
–> acute therapy and prophylaxis to include medication regiment and sfx
comfort measures (dark place, quiet)
Surgical management of seizures
Lobectomy
Resection surgery
Stimulator
Bacterial meningitis infectious agents
Streptococcus pneumoniae and Neisseria Meningitidis
Bacterial meningitis risk factors
Tobacco use Mastoiditis Immunosuppressed Young or Old Low GCS
Bacterial meningitis: treatment
Antibacterial (penicillin, IV dextramethasone), anticonvulsants
Bacterial meningitis: clinical manifestations
HA Fever Stiff neck (nuchal rigidity) ALOC PositiveKernigsign Positive Brudzinski sign
What does the nurse recognize as expected findings in a client with bacterial meningitis
The nurse recognizes that with fever, tachycardia and tachypnea are expected.
If bradycardia and decreased RR are seen, the nurse should consider ICP as an etiology for the decreased HR and RR.
What is a positive Kernig sign
When the patient is lying supine with the hip flexed to a 90-degree angle, resistance to passive extension of the knee is a positiveKernigsign
This pain is caused by inflammation of the meninges and spinal roots.
What is a positive Brudzinski sign
When the patient’s neck is flexed (after ruling out cervical trauma or injury), flexion of the knees and hips is produced; when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity
What meningitis is more common and what one is more deadly
common - viral
deadly - bacterial
What is common with viral meningitis?
HIV and children
Clinical manifestations of viral meningitis
HA low grade fever stiff nech photophobia malaise URI NO ALOC or sz.
What is the biggest difference between viral and bacterial meningitis
with viral, you will see no sz. and no AMS but you will see that with bacterial
Viral meningitis treatment
HOB 30
dark quiet room
isolation (both types)
Encephalitis
acute inflammation of brain tissue
Herpes Simplex Encephalitis impacts what
olfactory and trigeminal nerves - common pathways
Herpes Simplex Encephalitis: s/s
HA, Fever, Stiff neck & confusion
Herpes Simplex Encephalitis: tx
Acyclovir
Arboviral encephalitis - cause
misquito
Arboviral encephalitis: s/s
Flu-like, can have HA and nuchal rigidity, SIADH, rash
What is Bell’s palsy
facial paralysis
Bell’s Palsy: s/s
increased lacrimation Painful sensations in the face Ear pain Speech difficulties Smiling – absence of wrinkling on the forehead Mask-like face
Bell’s palsy: treatment
Corticosteroid therapy
Heat to help blood flow
Eye ointment –> lid can not close because they can not blink
Multiple Sclerosis
Destruction of the myelin that surrounds certain nerve fibers about brain and spinal cord – therefore impairing impulse
Multiple Sclerosis: primary symptoms
Unilateral visual loss Fatigue Depression Weakness Limb numbness Difficulty with coordination Loss of balance Pain (nerve fibers open)
Think fatigue and loss of coordination d/t destruction of myelin –> impairs impulses
MS: treatment
Interferon beta-1a and interferon beta-1b
Promote physical mobility (rest right before they become too fatigued, no strenuous)
Bowel/bladder training
Coping
Myasthenia Gravis: what
Autoimmune disorder – muscle weakness of voluntary muscles
Myasthenia Gravis: s/s
Diplopia
Weakness with muscles in the face/throat
Dysphonia
Motor Dysfunction only – no effect on sensation or coordination
Muscle weakness, intensifies with activity, improves with rest
Myasthenia Gravis: Treatment
Acetylcholinesterase test – diagnose Ice pack over eyes for 2 minutes Pyridostigmine bromide Corticosteroids Caution at dentist office with Novocain
What is the neurotransmitter that plays a big role in myasthenia gravis
acetacholine
Nursing management: MG
Meals coincide with the peak anticholinesterase medications
Patient must sit up right during meals
Soft foods
Suction available
Supplemental feedings
Impaired vision – tape/patch eye closed
Avoid stress factors – emotional stress, infections (respiratory), vigorous exercise, high environmental temperatures
Rest throughout the day
Myastenic crisis
Temporary exacerbation of s/s
Respiratory weakness
Cholinergic crisis
Muscle weakness
Respiratory impairment
Excessive pulmonary secretions
Guillain-Barre Syndrome
Autoimmune attack on peripheral nerve myelin
Rapid, acute, segmental demyelination of peripheral nerves
Typically happens about 2 weeks after an infection
What are big characteristics of Guillain-Barre Syndrome?
Dyskinesia, Hyporeflexia, and paresthesia
Guillain-barre syndrome s/s
Muscle Weakness
Sensory impairment
Depending on how far up the symptoms go – complications
Does not affect cognitive function or LOC
Guillain-Barre Syndrome: tx
IVIG
Plasmapheresis
Guillain-Barre Syndrome: nursing considerations
medication ER Monitor respiratory function Physical Mobility Adequate Nutrition Improving Communication Fear and Anxiety – include Family
Parkinson’s disease
Slowly progressing neurological Movement
Decreased levels of dopamine – leaves more excitatory neurotransmitters
Symptoms appear after 60% neurons are lost
Parkinson’s s/s
Tremor Rigidity Akinesia/Bradykinesia Postural disturbances Uncontrolled sweating, orthostatic hypotension, urinary retention, constipation Cognitive changes Sleep disturbances
Parkinson’s treatment
Levodopa with Carbidopa
Nursing management for parkinson’s disease
Improve mobility Self-care Bowel Elimination Nutrition & Swallowing Communication Coping
Alzheimers disease
most common type of dementia. This disease is a progressive, irreversible, degenerative neurologic disease that begins insidiously and is characterized by gradual losses of cognitive function and disturbances in behavior and affect
Alzheimers disease s/s
Forgetfulness
Subtle memory loss
Personality changes
Alzheimers: tx
Cholinesterase inhibitors - donepezil hydrochloride (Aricept), rivastigmine tartrate (Exelon), and galantamine hydrobromide (Reminyl), enhance acetylcholine uptake in the brain, thus maintaining memory skills for a period of time.
Memantine (Namenda) is an N-methyl-D-aspartate receptor antagonist that is thought to interfere with glutaminergic overstimulation.
Alzheimers: nursing management
Safety
Support
Self-care
Reducing Anxiety/Agitation
