MOD 11 Flashcards
Levels of consciousness from most concious to least concious
alert and oriented
confused
lethargy
obtundation
stupor
coma
Unconsciousness related to death
cerebral death: an irreversible coma or a persistent vegetative state
Brain death: absent cerebral function and unable to maintain physiologic homeostasis
cognition
means thinking skills that include awareness, language calculation and memory
dementia
organic brain degeneration, progressive, untreatable, irreversible decline in mental functiond
delusion
false belief brought about without appropriate external stimuli (unrelated to reality)
delirium
acute reversible state of agitated confusion. Disorientated to time and place with hallucinations usually symptomatic of a disease and is reversible with treatment of the disease can be caused by a high fever
GCS
Glasgow coma score
scale that helps gauge the impact of a wide variety of conditions affecting the patient’s level of consciousness
lowest possible score a patient could receive of GCS
a 3 for none
pathologic posturing
painful stimuli indicate serious brain damage.
abnormal flexion = decorticate
abnormal extension = decerebrate posturing
acute brain damage GSC measures
trauma
vascular injuries
infections
hypoxia
metabolic disorders
decorticate posturing
indicates that there may be damage to the vertebral hemispheres and possible midbrain
limbs point to the core of the body
Decerebrate posturing
usually indicative of more severe damage indicating a lesion in the cerebellum or lower in the brainstem. very poor prognosis
hands point away from body = brain has gone away
Flaccid paralysis
characterized by limp (floppy) unresponsive muscles that cannot contract. Can be caused by infections and toxins or damage to the spinal cord or brain
Blood-brain barrier
a network of blood vessels that allows the entry of essential nutrients while blocking other substances. The blood vessels are lined with endothelial cells that are wedged tightly together creating a nearly impermeable boundary between the brian and bloodstream
The downside to blood-brain barrier
it is so effective at protecting against the passage of foreign substances that it often prevents life-saving drubs from being able to repair the injured or diseased brain
most dangerous outcome of cerebral edema
increased ICP due to brain injury.
what is the most serious complication of a head injury
cerebral edema or bleeding which can result in increased intracranial pressure.
Vasogenic edema
blood-brain barrier damage causes increased capillary permeability. This occurs with conditions that impair the function of the blood-brain barrier and allow the transfer of water and proteins from the vascular space into the interstitial space leading to swollen brain tissue
Cytotoxic edema
the blood-brain barrier remains intact but a disruption in cellular metabolism impairs the functioning of the sodium-potassium pump active transport failure leads to K+ loss and Na+ retention increasing cellular H2O which leads to ischemia of brain tissue and necrosis of brain cells.
Treatment for cerebral edema
position the patient with the head of the bed elevated 30 degrees
Hypertonic IV fluids pull fluid out of the brain (hypertonic saline and mannitol)
Diuretics- medication to increase the production of urine, and help reduce fluid overload
corticosteroids- suppress the inflammatory response and reduce swelling in the brain
surgical decompression- removing part of the skill allows the brain to swell without being compressed
Increased intracranial pressure (ICP or IICP)
include rise in cerebrospinal fluid pressure, increase pressure within the brain matter, bleeding in and around the brain, swelling.
the pressure can damage the brain or spinal cord by pressing on important brain structures
Early signs of ICP
decreased LOC
pupil changes: perrla (pupils equal, round, reactive to light, and accommodation)
vision abnormalities
headache
vomiting
nuchal rigidity- stiff neck
late sign of ICP
impaired reflexes
papilledema (optic disc swelling)
abnormal posturing (decorticate/ decerebrate)
Cushing’s triad
hypertension (widening pulse pressure- difference between the systolic and diastolic b/p increases)
bradycardia
hypoventilation leading to hypercapnia which causes vasodilation
Primary brain injury
focal injuries- contusions, hematoma’s
diffuse injuries- concussions; diffuse axonal injury; traumatic subarachnoid hemorrhage
secondary brain injury
cause damage to parts of the brain that were not initially injured
damage caused by the inflammation process
swelling leads to ICP leads to brain herniation leads to tissue necrosis
S/s of head injury and TBI
loss of consciousness
headache
vomiting
drowsy
confusion
seizure
drowsiness
restlessness
agitation
LOC changes
contralateral hemiplegia
ICP signs of herniation
check for what with a head injury and TBI
fluid draining from ears and or nose with a glucometer for the presence of glucose
Points to remember with a head injury and TBI
H.I can result from a ground level fall, especially in the elderly
assume “C-SIPINE INJURY” will occur with any H.I. (do not move injured person)
Nursing care for H.I. and TBI
frequent assessment of LOC (using GCS) keep patient’s head elevated 30 degrees to prevent intracranial pressure
NOTE: an order that reads: HOB 30 degrees means “keep the head of the bed up 30 degrees”
protect airway keep suction equipment at patient’s bedside due to vomiting
Concussion
no gross pathology
possible transient loss of consciousness
CT scan is normal
Post-concussion syndrome s/s are headaches and memory lapses
contusion
bruising of the brain surface underneath a fracture or at the under-surface of the frontal temporal lobes, due to shearing forces. diagnosed on ct scan.
Laceration
tearing of the brain substance.
diagnosed by ct scan
Brain/cerebral edema
this is localized in the glial cells, myelin sheaths, and intercellular spaces. it causes increased intracranial pressure, which may impair brain circulation, or result in brain herniation, it may be missed in early CT scans. Later CT scans or MRI show edema more reliably
Herniation
displacement of brain tissue towards the other side of the brain which increases pressure on the non-injured side. the further the brain tissue has herniated “passed midline” the worse the prognosis
Acceleration-deceleration head injury
“coup-contrecoup” hitting both front and back of the head results in brain conditions and hematomas (more than one injury from the same blow)
Cerebrovascular infarction
focal brain necrosis due to complete and prolonged ischemia that affects all tissue elements (neurons, glia, and vessels) in every infarct, there is a central core of total ischemia and necrosis, which is irreversible
Epidural hematoma
blood clot that forms between the skill and the top lining of the brain (dura) this blood clot can cause fast changes in the pressure inside the brain. Usually an arterial bleed so can expand very quickly.
early sign of epidural hematoma
Ipsilateral pupil dilation (dilation of pupil on the same side as the brain hematoma)
Subdural hematoma
blood clot that forms between the dura and the brain tissue. if this bleeding occurs quickly it is called an acute subdural hematoma. if it occurs slowly over several weeks, it is called a chronic subdural hematoma. The clot may cause ICP and may need to be removed surgically.
Intracerebral hematoma
a blood clot deep in the middle of the brain that is hard to remove. Pressure from this clot may cause damage to the brain. Surgery may be needed to relieve the pressure. Can be either arterial or venous
Alzheimer’s disease
etiology: excessive decline in first mental and then physical abilities. Most common form of dementia (accounts for 60-80% of dementia cases)
Alzheimer’s is the sixth leading cause of death in the United States. Those with Alzheimer’s live an average of 8-10 years. but survival can range from 4-20 years.
Alzheimer’s = type 3 diabetes
alzheimers gene seems to interfere with brain cells’ ability to use insulin which may eventually cause the cells to starve and die.
stages of Alzheimer’s
first: short-term memory loss
second: confusional stage
third: incontinence; long-term memory loss (inability to recognize family and friends)
Alzheimer’s RF
Age, Heredity (genetic predisposition), and FAMILY HX
Hispanics and African Americans, there is a connection between heart health and brain health
diabetes, high b/p, and high cholesterol might lead to stroke-related dementia.
Pathophysiology of Alzheimer’s
neuronal proteins develop into neurofibrillary tangles. causes areas of degenerated tissue called SENILE PLAQUES. These plaques impair transmission of neural impulses.
Incidences of Alzheimer’s
familial Alzheimer’s disease - “FAD” or early-onset Alzheimer’s - 30% of cases, occurs before 50 yrs
nonhereditary (late-onset) Alzheimer - 70% of cases; occurrence after age of 50
s/s of Alzheimer’s
mental changes begin with recent memory loss and then progress to remote memory loss. Signs of mental damage precede the physical signs of illness progression.
main groups of s/s of alzheimers
cognitive
behavioral
mood
psychological
also common is restlessness, behavioral s/s, loss of appetite, inability to combine muscle movements, or jumbled speech
Rx of alzheimer’s
supportive care to maintain function. Medication is sometimes helpful to slow the rate of mental loss but will not cure or prevent the ongoing decline in either mental or physical symptoms.
Cerebrovascular accidents
CVA, Brain attack, or stroke
Etiology for brain attack (CVA or stroke)
may be caused by thrombi, emboli, or hemorrhage
Ischemic Thrombotic CVA
patho: thrombi cause arterial occlusion (narrows blood vessel) = MOST COMMON
S/s: acute onset (hrs to days), occasional HA, no LOC, +Hx, TIA’s
Rx: decrease edema and ICP
Embolic CVA
Patho: emboli break off from thrombi in the aorta or carotids
S/s: acute onset, often moderate HA, occasional brief LOC, no Hx TIA’s
Rx: anticoagulants, eliminate cause
Hemorrhagic CVA
Patho: hypertension, aneurysm, or ruptured vessels
s/s: Acute onset, Severe HA, + stiff neck, + LOC, + blood in cerebral spinal fluid
Rx: stop bleed, decrease ICP and vasospasm (no anticoags)
Non-modifiable RF for stroke-brain attack
non-modifiable:
having fx or stroke
being 55 or over
more than half stroke occur in men
black and Hispanic
prior stroke, TIA (transient ischemic attack) or heart attack
Modifiable RF for stroke
High b/p
smoking
atherosclerosis
diabetes
atrial fibrillation
overweight-especially abdominal fat
lack of exercise
overconsumption of alcohol
FAST recognition of stroke
F: face (are both sides equal? is the smile equal?)
A: arms (can the client raise both arms equally)
S: Speech (is speech slurred? can the client make a sentence)
T: Time (get help now. There is a small window of opportunity)
Excess belly fat increases risk of what
increase the risk of stroke by 4 times.
Aphasia
can be caused by CVA it is the loss of comprehension or production of language that impairs the patient’s ability to communicate
Expressive aphasia
patient understands what is being said to them but cannot speak (or express themselves) coherently
Receptive aphasia
The patient can speak coherently but does not understand (is not “receiving) what is being said to them
Stroke treatment
time is vital in saving brain tissue, thrombolytic medication, must generally be given within 3 hours of onset of symptoms.
TIA’s names
transient ischemic attack
aka “mini stroke”
“angina of the brain”
Thrombolytds can be given for what kind of stroke
Ischemic stroke
NOT
hemorrhagic
TIA definition
brief episodes of neurologic dysfunction. can have all the s/s of a stroke but reverses before infarction occurs.
Temporary, resolved without treatment, NO PERMANENT DAMAGE.
TIA’s precede what
thrombotic brain attack, 1 in 3 people who have transient ischemic attack will eventually have a stroke.
Pathophys of SCI
spinal cord injury
Trauma, tumors, concussion, contusion, compression, tearing, or ischemic injury to the spinal cord with or w/o vertebral damage.
S/s of cervical spine injury
quadriplegia (paralysis that results in the partial or total loss of use of all limbs and torso)
S/s of thoracic spine injury (T1-T7)
paraplegia (impairment in motor or sensory function of the lower extremities)
S/s C1-C3 injury
requires mechanical ventilation of the patient
Spinal shock s/s
all reflexes including somatic and autonomic are temporarily lost below the level of injury. 1-3 weeks but may be up to 3 months. resolves as edema/ injury resolves. could have HYPER reflexia for another year after sensation returns
Compressed spinal cord injury
spinal cord remains intact but could be confused (bruised) and swollen, thereby preventing conduction of nerve signals below the point of injury.
Transected spinal cord injury
the spinal cord is completely severed
Incomplete spinal injury
Some function is preserved only a portion of the spinal cord may be injured. prognosis for return of function is better in an incomplete because of preservation of axonal function
Involuntary anal reflex
contraction of the anus when lightly touched (called the “anal wink” if this reflex is present in a person paralyzed after a SCI, chance of recovery is better than if the reflex were absent
Complete Spinal injury
All Function - is lost below the damaged spinal cord
cause of complete spinal injury
spinal cord severed (transected) disruption of nerve fibers although they may remain intact; or interruption of blood supply to a segment or spinal cord resulting in complete destruction of neural tissue.
s/s of complete spinal injury
because there is no motor nerve communication with the brain: flaccid paralysis, and loss of vasomotor tone can result in severe low b/p or bradycardia depending on the level of injury
Autonomic Dysreflexia
common with patients with spinal cord injury at T6 and above
causes of autonomic dysreflexia
dangerously high blood pressure - can be high enough to cause a stroke or seizures
often triggered by a noxious stimulus below the spinal cord injury such as a full bladder
Autonomic dysreflexia pathophys
this strong sensory input travels up the spinal cord and evokes a massive reflex sympathetic surge from the thoracolumbar sympathetic nerves, causing widespread VASOCONSTRICTION usually below the level of injury so peripheral arterial hypertension
sympathetic nerves prevail at what
below the level of neurologic injury
parasympathetic nerves prevail at what
above the level of the injury
sympathetic response causes
vasoconstriction below the injury
parasympathetic nerves cause what
vasodilation above the injury
the vasoconstriction below the injury causes
hypertension, pounding headache, visual changes, anxiety; pallor; and goose bumps below the level of injury
Symptoms of autonomic dysreflexia
HTN (due to vasoconstriction)
a slow heart rate (bradycardia) to compensate for HTN
Above the injury (parasympathetic) s/s
vasodilation
flushed face above the level of spinal injury
nasal congestion
headache
sweating above the level of spinal injury
Below the injury (sympathetic) s/s
pale, cold, clammy skin below the level of injury
goose bumps below the level of spinal injury
Meningitis (bacterial)
usually from direct exposure or systemic bacteremia - the most serious form of meningitis - can cause long-term and or permanent brain damage/death. Hogh mortality rate
Meningitis (viral)
aseptic - usually from upper respiratory infection - the most common cause of meningitis and usually the least severe. often resolves in 2 weeks without treatment
Meningitis (fungal)
usually found in immunosuppressed individuals
Meningitis pathophysiology
infection of the meninges, droplet precautions, CSF, and ventricles become inflamed leading to obstruction of CSF flow, edema of infected tissues and potential ischemia due to increased ICP
Meningitis Rx
related to pathogen (antibiotic or antifungal meds): vaccination is available against some pathogens
Incidence of meningitis
viral is most common; bacterial is most severe
s/s of meningitis
throbbing headache
nuchal rigidity (stiff neck)
fever
photophobia
projectile vomiting
altered LOC
increased ICP
red purpuric or blotchy rashes that do not blanch when applying pressure
kernig’s sign and/or brudzinski’s sign may be present
meningism
term used for a group of s/s that are commonly present (but not always) when the meninges are irritated, as in infection (meningitis) subarachnoid hemorrhages, or other diseases
suggestive s/s of meningeal irritation
photophobia
nuchal rigidity
opisthotonus
kernig’s sign
brudzinski’s neck sign
