Module 3 Exam 1- Neuro Flashcards
treatment for acute seizure
ativan (lorazepam)
nonacute seizure medications
depakote, phenytoin
complications of cerebral injury
DVT, pneumonia, hypotension, urinary retention
intracranial surgeries
craniotomy, burr holes, cranioplasty, craniectomy
craniotomy
opening at the skull; used to remove tumors, relieve elevated ICP, evaluate blood clot, control hemorrhage
burr holes
circular openings in the skull; used to provide access to ventricles, shunting procedures, hematoma or abscess, bone flap
cranioplasty
surgery to reconstruct bone defects in the skull
craniectomy
surgery to remove portion of skull; used to alleviated increased ICP
neuro preop care assessment
monitor vitals and LOC; monitor ABGs, ICP; monitor fluid status in labs; monitor for seizures (give meds if needed); monitor for signs and symptoms of infection (give antibx if needed) and complications
diagnostic procedures for neuro
CT scan, MRI angiography, transcranial doppler flow studies
levels of traumatic brain injuries
concussion = mild; contusion = moderate/severe; diffuse axonal injury (DAI) = severe
concussion
mild TBI; sudden trauma induced alteration at the alert state; may or may not experience brief LOC; may or may not experience brain bleed, swelling, or skull FX
contusion
moderate to severe TBI; bruising of the brain; experience LOC with stupor and confusion; injury may be at site of impact or opposite side (damages cortex); large contusions may be surgically removed
diffuse axonal injury (DAI)
severe TBI; deceleration injury from differential movement of brain and skull; axonal shearing; high mortality rate; posturing
decorticate posturing
damage to corticospinal tract (cortex lesion); pathway between brain and spinal cord; rigid extended legs, pointed toes, curled wrists, balled hands against chest
decerebrate posturing
severe injury to the brain at level of brainstem; poor prognosis; rigid extended legs, pointed toes, straight tense arms parallel to body, flexed wrists, curled fingers
epidural hematoma
between the skull and the dura results from trauma; momentary unconscious, then lucid period, then confusion, then coma; “talking die syndrome”
subdural hematoma
venous bleed between dura and brain caused by trauma; dilated pupils and fixed, headache, drowsy, confusion, hemiparesis; intervention is immediate craniotomy and evacuation of clot
intracerebral hematoma
bleeding withing brain seen when force exerted to head over small area (ex. bullet, stab); insidious onset progressing to headache and then neurologic deficits
subarachnoid hemorrhage
cause by head trauma, ruptured cerebral aneurysm, arteriovenous malformation (AVM)
signs and symptoms of subarachnoid hemorrhage
severe headache suddenly that worsens and is worse in back of head; “worst headache of life”; decreased LOC; photophobia; confusion and irritability; N/V; muscle aches, stiffness; seizures; diplopia, blindspots
treatment for subarachnoid hemorrhage
remove collection of blood to relieve pressure; repair aneurysm
nursing care of spinal cord injury loss of muscle function
maintain ABCs; keep pt immobilized with c-collar, backboard, or halo; assess loss of function
nursing care of spinal cord injury cardiovascular
avoid vagal stimulation (careful with suction); monitor vitals; admin atropine to induce sympathetic response and vasopressors if needed; assess need for pacemaker; admin fluid and blood to maintain SBP >90 and MAP > 65; vagal stim can cause brady and then arrest
neurogenic shock
acute injury to brain, cervical, or thoracic spine that causes distributive shock d/t loss of autonomic nervous system to control blood vessel; can occur 30 min - 6 weeks following injury
manifestations of neurogenic shock
hypotension, bradycardia, poikilothermia, anhidrosis
treatment for neurogenic shock
spinal stabilization, vasopressors, atropine, pacemaker
patho of neurogenic shock
loss of SNS tone, massive vasodilation and venous pooling, hypotension, low perfusion, cell death
GI/GU affected from spinal cord injury
neurogenic bladder and bowel due to disrupted innervation; no signal to go leads to either incontinence or retention or paralytic ileus; spastic bladder;
nursing care for spinal cord injury GI/GU
intermittent foley cath q4 hr; digital rectal exam or stimulation- enema, stool softener, fiber, water; medications like H2 blocker (famotidine), PPI (omeprazole), metoclopramide (reglan)
nursing care spinal cord injury metabolic/nutrition
nutritional support d/t high cal demand, anorexia from depression, and atrophy; parlytic ileus; monitor fluids, electrolytes, ABGs (sodium and potassium) \; feed via NG, G, or TPN within 24-48 hrs; ETT, Trach, NG tube- risk for metabolic acidosis
autonomic dysreflexia
SNS below level or injury responds to stimulus of sensory receptor and hyperstimulates SNS, vasoconstricts, and causes HTN; no opposition from PNS from spinal cord; PNS stimulated throgh baroreceptors in carotid arch and causes bradycardia and no vasodilation
manifestations of autonomic dysreflexia
HTN with throbbing headache, blurry vision, diaphoresis above SCI, bradycardia, piloerection (aka goosebumps), flushing above SCI
treatment of autonomic dysreflexia
remove stimulus by intermittent cath, removing fecal impaction, removing pain trigger; lower BP with nifedipine which is calcium channel blocker
poikilotherma
inability to sweat/shiver or control temperature; occurs below SCI
nurse treatment for poikilothermia
control external temperature; vital signs frequently
nociceptive pain
musculoskeletal and visceral pain controlled via tylenol, ibuprofen, opioids
neuropathic pain
nerve pain controlled with gabapentin, pregabalin
complications of skin and reflexes from SCI
immobility- at risk for DVT, PE, decubiti; hyperactive reflexes
treating skin and reflex complications from SCI
LMWH/Warfarin, repositioning, logrolling for DVT and PE; repositioning q2 and logrolling for decubiti; baclofen, ROM, PT/OT for hyperactive reflexes
complications of SCI
pain, spinal sock, neurogenic shock, skin, reflexes, thermoregulation, metabolic/nutrition, cardiac, muscular, respiratory
spinal shock
occurs 24hrs-6 weeks after injury; complete but temporary loss of motor function, sensation, autonomic activity; brain unable to transmit signals to muscles and organ
manifestations of spinal shock
flaccid paralysis, clonus (first sign), no DTR, low visceral/somatic sensations, anhidrosis, parlytic ileus
treatment of spinal shock
spinal stabilization, maintain ABCs, Pt and OT
anhidrosis
absence of sweating
respiratory complications with SCI
total loss of respiratory function if C4 or higher-phrenic nerve injured; Lower C or T spin affects intercostal muscles and abdomen leading to hypoventilation, long term causes secretions, pneumonia, atelectasis;
nursing care of respiratory SCI
obtain breath sounds and monitor for hemothorax, monitor breathing patterns, care of ETT and tracheostomy, encourage cough deep breathing and incentive spirometer
cushing triad
signs of a brain injury consisting of hypertension (widened pulse pressure), bradycardia, and irregular respirations
somatic
voluntary muscle and skeletal
autonomic
involuntary-automatic; consist of the unconscious; sympathetic and parasympathetic
sympathetic
fight or flight
parasympathetic
rest and digest
hypothalamus controls
HR, BP, sleep
brain stem
consist of midbrain, pons, medulla- controls respiration, heart, GI, CN 8-12
cerebellum
controls motor and sensory integration, coordination, fine movement, balance
mean arterial pressure
depends on BP and chemicals like CO2; normal is 70-100; below 60 mmHg- peripheral organs not perfused; below 50mmHg- brain not perfused; need to maintain normal MAP with increased ICP
autoregulation of the brain
ability of the brain to maintain relatively constant blood flow despite changes in perfusion pressure; maintained by cerebral blood flow and cerebral arterioles
neurological assessment
consists of subjective and objective data; physical exam looking at mental status, motor system/cerebellar function, sensory system, DTR, cranial nerves
motor system/cerebellar function consists of
gait, muscle coordination, muscle strength (5 point scale), atrophy, tremors
sensory system consists of
pain, temperature, proprioception
altered LOC on GCS
minor injury- 13-15, moderate injury- 9-12, severe injury- 3-8; intubate at 8; 3 is brain death
altered LOC is considered…
any measure of arousal that is not normal
normal intracranial pressure
0-15mmHg (15 is high end of normal)
if ICP is sustained over 20mmHG
brain injury issues will arise
cerebral perfusion pressure (CPP)
the pressure needed for adequate blood flow to the brain; CPP = MAP - ICP
CPP ranges
70-100mmHg is normal; <60mmHg is sign of ischemia; <50mmHg is sign of death
how to manipulate cardiac output for brain perfusion
fluid volume and inotropic agents like dobutamine and levophed
venticulostomy
how we measure ICP; catheter placed into ventricle; decrease ICP by releasing CSF; continuously measures ICPc
complications of ventriculostomy
infection, meningitis, occlusion, ventricular collapse
caring for ventriculostomy
1 inch above (too high = less drainage; too low = increased drainage); maintain asepsis, monitor for bleeding and CSF leakage; monitor vitals; monitor WBC; monitor drain site and assess for drainage; monitor for over drainage (headache), HOB at 30 degrees
causes of increased ICP
mass, lesions, cerebral edema, increased CSF production, decreased CSF absorption, obstructive hydrocephalus, obstruction of venous flow
early signs of increased ICP
decreasing LOC, headache and increased sensitivity (worse in AM), restlessness, contralateral muscle or sensation loss, pupillary change (fixed, dilated, unequal, diplopia, ptosis), changes in speech
late signs of increased ICP
further decrease in LOC, fever without clear source, projectile vomiting, changes in vitals such as increased SBP and decreased DBP (widened pulse pressure), bradycardia, bradypnea, bilateral pupil dilation, loss of corneal and gag and swallow, posturing
complications of increased intracranial pressure
brain stem herniation, diabetes insipidus (DI - dry inside), syndrome of inapropriate antidiuretic hormone, cushings triad
treatment of diabetes insipidus from increased ICP
fluids, electrolytes, vasopressin, monitor I/O
treatment of inappropriate antidiuretic hormone
electrolytes, restrict fluid, monitor I/O
patho for diabetes insipidus
lack of anti-diuretic hormone (vasopressin) causes body to not hold onto water and results on lots of urine creating a dry inside
nursing interventions for increased ICP
patent airway, monitor RR and O2, adequate cerebral tissue perfusion, normalize respirations, fluid balance, absence of infection, absence of complications, seizure precautions, treat pain
management of increased ICP
decrease cerebral edema, lower volume of CSF, decrease blood volume but maintain cerebral perfusion; admin osmotic diuretics to dehydrate brain and reduce cerebral edema like mannitol
