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
