Exam 3 - Neuroscience Flashcards
LOC, ICP, Spinal cord injury, buillian barre
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Arousal
Brainstem pathways (RAS) governing wakefulness
Awareness (content)
Cerebral functions including thought behavior, language, expression
Continuum of Consciousness levels
Alert Confused Lethargic Obtunded Stuporous Comatose
Alert (conscious)
attends to environment; responds appropriately to commands question with minimal stinulation
Confused
Disoriented to surroundings; may have impaired judgment; may need cues to respond to commands
Lethargic
Drowsy, needs gentle verbal or touch stimulation to initiate a response
Obtunded
Responds slowly to external stimulation; needs repeated stimulation to maintain attention and response to the environment
Stuporous
Responds only minimally with vigorous stimulation; may only mutter or moan as verbal response
Comatose
No observable response to any external stimuli
Consciousness depends on the
Reticular activating System (RAS)
Focused exam for critical/emergent pts
LOC Motor function pupils/eyes respiratory/ airway function vital signs
Components of the neurological assessment
- Neurological Hx
- Physical Exam
- LOC
- Motor function
- Pupillary changes
- VS
- Cranial nerves
Most important and critical indicator of cerebral function
LOC
Consciousness is dependent on the ____
RAS - Reticulating activating system
LOC assessment
- Consciousness
- Glascow coma scale
- stimulus-reaction level scale
Motor function Assessment of Coordination
Romberg test
Finger to nose
Rapidly alternating movement (RAM)
Motor Response assessment
Decorticate: abnormal flexion (core)
Decerebrate: abnormal extension (E)
Flaccid
Babinski: abnormal in adults (curl=norm, flare=abn)
Cranial Nerve assessment
- Pupils (especially helpful in unconscious client)
- CN3 (EOM) awake client only
- CN3: midbrain, one of the first to be compressed
Oculocephalic Reflex
“Doll’s eyes”
- Unconscious pt without spine injury
- Opposite = Good
- Same = Bad
Oculovestibular reflex
Checks to see if brain stem is intact
-NEED INTACT TYMPANIC MEMBRANE
-unconscious pt
irrigate each ear w/ 30-50mL iced water with pt supine and HOB at 30 degrees
-Normal = eyes move slow toward painful stimulus followed with rapid movement away from stimulus
-Abn=absent reflex, eyes remain midline
Cranial nerves
CN IX: gag, cough,
CN XI & XII: must be alert (swallow, shrug shoulders)
Abnormal Respiratory Patterns
- Cheynes-Stokes
- Central neurogenic hyperventilation
- Apneustic breathing
- Cluster breathing
- Ataxic breathing
Late VS changes
BP has increased pulse pressure
HR and rhythm:bradycardia common
ICP
Pressure exerted within the cranial vault by brain tissue, CSF, or Blood
Monro-Kellie Doctrine
an increase in any one of the contents in the brain is accompanied by a reciprocal change in the volume of one of the others:
blood 10%
CSF 10%
Brain 80%
The compartments BEST able to be manipulated to buffer changes in IICP volume
Blood & CSF
Normal ICP Range
0-15 mmHg
Indications for ICP monitoring
- GCS of <8 or GCS motor scale +/- 5 (ex: not following commands)
- Need to assess response to interventions
- Increased volume of brain, blood, or csf
Causes of IICP
- Impaired auto regulation of cerebral blood flow
- head injury, Reye’s syndrome, Encephalitis, Asphyxia - Cytotoxic Edema
- Head injury, Toxins, Asphyxia - Mass/Lesion
- Tumor, bleeding, Abscess - CSF obstruction: hydrocephalus, mass, lesion, or meningitis
- Hyperosmoalr states: DKA, HHNS, hypernatremia
Activities that increase ICP
- Valsalva
- Emotional stress
- Noxious stimuli
- Suctioning
- Fever
- Pain
- REM Sleep
- Cough
- Sneeze
- Vomiting
- Flexion
- Fart
Normal cerebral blood flow
is 15% of cardiac output, consuming 20% of total O2
Cerebral Perfusion Pressure (CPP)
CPP= MAP - ICP
Herniation syndromes - Cingulate
shift of brain tissue from one cerebral hemisphere to the other
Herniation syndromes - Central
Downward shift of cerebral hemispheres thru tentorial notch, compressing vital centers of brain stem
Herniation syndromes - Uncal
Uncus of temporal lobe displaced thru tentorial notch, compressing MIDBRAIN
MOST SERIOUS COMPLICATION OF IICP
Early signs of IICP
RESTLESSNESS
change in LOC
HA
Pupillary changes (mild, sluggish actually a late sign)
Contralateral motor or sensory loss (opposite side)
Late signs of IICP
Further decrease in LOC Papiledema pupillary changes Changes in VS Cushings triad Changes in respiratory pattern Fever Projectile vomiting POSTURING Loss of reflexes
Cushing’s Triad
Increased SBP
Decreased DBP (widened pulse pressure)
Bradycardia
Ventriculostomy - Intraventricular catheter
a procedure for measuring ICP by placing an ICP monitor within one of the fluid-filled, hollow, chambers of the brain, called ventricles. These four natural cavities are filled with csf which also surrounds the brain and spinal cord
ICP monitoring, maintained as closed system to avoid infection, maintain transducer at EAR LEVEL, must zero
-NEVER FLUSH
Subarachnoid bolts/Screw
ICP monitoring, placed in subaranoid space
Direct measurement for CSF
Access for volume-pressure responses
Access for CSF drainage and sampling
Epidural Sensor
Placed between skull and dura
LEAST INVASIVE
ACCURACY UNCERTAIN
Intraventricular catheter
Inserted into Anterior horn of lateral ventricle
MOST INVASIVE
MOST ACCURATE
Higher risk for INFECTION & ICH
ICP Monitoring
Infection is a serious concern
ICP 20-25 mmHg needs Tx
ICP >60 mmHg is fatal
ICP is measured at END OF EXPIRATION, q2-4hr
Nursing care for ICP Monitors
- Sterile dressing and sterile technique
- Monitor site for drainage
- ZERO and maintain at FORAMEN OF MONRO (outer corner of ear)
- NEVER FLUSH when connected to hemodynamic system
Nursing care for IICP
- Intubation
- Sedation: Versed/Ativan
- Elevation of HOB, head midline
- Meds: mannitol, antiseziure, neuromuscular blockade agents, barbiturate coma
- TX like “mushrooms” cool dark quiet room
Mannitol
Decreases blood viscosity, acts as osmotic agent to decrease brain water with osmotic diuresis
Complications of ICP pressure devices
- Hemorrhage
- Infection
- CSF leakage
- Hematoma
TBI Primary Injury Patho
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TBI Secondary Injury Patho
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Primary Injuries - TBI
- Concussion
- Contusion
- Laceration
- Diffuse Axonal Injury (DAI)
Concussion
mechanical force of short duration applied to skull, results in temporary failure of impulse conduction. Neurological deficits are reversible and general mild.
May lose consciousness for a few seconds at time of injury, lasting effects are not common
Contusion
Result of a coup and countercoup injury, accompanied by bruising and generalized hemorrhage into brain tissue. S/S are variable.
Lacerations
Involve actual tearing of the brain tissue and occurs frequently with depressed and compound fractures and penetrating injuries. Tissue damage is severe and surgical repair is impossible because of the texture of brain tissue
Diffuse Axonal Injury (DAI)
TWISTING AND TURNING OF THE BRAIN TISSUE AT THE TIME OF INJURY
Widespread axonal damage occurring after a mild, moderate ore severe tbi. damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus and brainstem.
DAI Dx tool of choice
MRI
Secondary injuries - TBI
- Ischemia (resulting from hypoxia and hypotension)
- Infection
Skull Fractures - Types
-Linear
-Comminuted
-Facial
-Basilar
-Depressed
Compound
Linear skull fracture
break in continuity of bone without alteration of relationship of parts, caused by low velocity injuries
Comminuted skull fracture
multiple linear fractures with fragmentation of bone into many pieces (egg shells), direct high momentum impact
Facial skull fracture
Involve facial bones
Basilar skull fracture
Fracture in the anterior middle and/or posterior fossa along the floor of the cranial vault. dura is torn
Depressed skull fracture
Inward indentation of skull caused by powerful blow to head
Compound skull fracture
depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity, caused by severe head injury.
Subdural hematoma (SDH)
Bleeding between dura and arachnoid layers, generally VENOUS in nature
Acute Subdural hematoma
S/S within 24-48hrs
Subacute subdural hematoma
S/S withing 28hr-2 weeks
Chronic subdural hematoma
within weeks to months
SDH Tx
Medical management of IICP
Burr holes
Surgical evacuation
Epidural Hematoma
Bleeding between dura and skull, generally ARTERIAL in nature
EDH Classic sign
Brief loss of consciousness followed by lucid interval then coma
Other S/S:
Ipsilateral pupil dilation, contralateral weakness, brainstem compression
MIDDLE MENINGEAL IS USUALLY THE ONE TO BLEED
Pt dies from brainstem compression
Intracerebral Hemorrhage (ICH)
Bleeding within the cerebral tissue that creates a mass lesion.
- due to closed head injury, aneurysm rupture.
- Treatment varies related to cause, extent and location of bleeding
Basilar skull fractures
Raccoon’s eyes and battle’s sign
At risk for MENINGITIS due to communicating pathway
Assessment of skull fx
- Neurological deficits and varying LOC
- CSF is positive for glucose, halo sign if blood present
Halo sign indicates
blood in csf
Assessment for meningeal irritation
- Brudzinski (stiff neck when flexed)
- Positive Kernig’s sign (cannot extend leg when thigh flexed on abdomen
- Photophobia
- Headache
- Fever
Interventions for Neuro pt
- Optimize oxygenation
- intubate/vent, control CO2 and O2 levels
- Suction only PRN, consider use of lidocaine to suppress cough - Control/reduce increased ICP
- icp monitoring & drainage
- reduce metabolic demands (sedation, seizure control, reg body temp, admin mannitol, lasix, steroid) - Monitor and prevent complications
- MONITOR I/O, URINE SPECIFIC GRAVITY FOR DI/SIADH
- ADMIN DVT/GI PROPHYLAXIS
- maintain bp
- hourly neuro checks
- ekg monitoring
DI
Not enough ADH, fluid volume deficit
Excessive UO, dilute urine
Blood is concentrated
SIADH
Too much ADG, fluid volume excess
Decreased UO, urine concentrated
Blood is dilute
Craniotomy
- Burr holes; circular openings in skull to evacuate hematomas, or to initiate more invasive brain surgery
- Craniotomy; surgical window in the skull made by sawing between multiple burr holes
- Supratentorial-access to areas above the tentorium
- Infratentorial- access to areas below the tentorium
Craniectomy
Surgical removal of a portion of the skull without replacement bone flap
Cranioplasty
Replacement of missing cranium with bone or plastic insert to restore skull contour and integrity
Craniotomy post-op care
- Avoid activities that increase ICP
- Watch for excessive post op drainage & notify physician at once
- neuro checks, LOC, pupils, movement and sensation
- elevate hob, position
- stool softener, diuretics, steroids, control temp and shivering
Subarachnoid Hemorrhage
Bleeding into the subarachnoid space between the pica and arachnoid layers of the Meninges.
- Cerebral aneurysm; weakening and abn dilation of a cerebral blood vessel
- Arteriovenous malformation (AVM); congenital malformation of cerebral arterial and venous blood vessels that connect directly, bypassing the capillary system; may produce increased ice; HIGHLY SUSCEPTIBLE TO RUPTURE
Clinical findings of SAH
Before bleed: HA, transient weakness, visual disturbances
After bleed: meningeal irritation, SEVERE HA, nuchal rigidity, N/V, PHOTOPHOBIA, seizures, fever, lethargy, kernig & brudzinski, DECREASED LOC
-neuro deficits
-visual changes due to retinal hemorrhage
-LABILE BP
SAH Complications
- Vasospasm (4-14 days after, peaks 7-10)
- Rebleed (3-11 days after, peaks at 7days)
- Hydrocephalus (acute or delayed)
Complete spinal cord injury (SCI)
total loss of sensory and motor function below level of injury
Complete quad
injuries above C6
Incomplete Quad
Injuries below C6
Paraplegia
Injuries in the thoracolumbar region
Incomplete SCI
mixed loss of voluntary motor activity and sensation below the level of the lesion
Central cord syndrome
arm paralysis
Brown-Sequard syndrome
motor loss on one side: pain, temp, touch loss on the opposite side
Anterior cord syndrome
motor loss, but retains light touch, proprioception and position
What is the predictor of complete vs incomplete lesion
Rectal tone
normal= squeeze
incomplete = weak squeeze
complete = flaccid
Spinal Shock
Flaccid paralysis, loss of sensation and reflexes below level of lesion
- absence of reflex activity; bowel or bladder
- loss of temp control
May last weeks to months, ends with return of reflexes and muscle spasticity
Neurogenic Shock
Interruption of descending sympathetic pathways causing vasodilation, resulting in hypotension and bradycardia
Potential Complication of SCI
Autonomic dysreflexia
hypoxia, dvt/pe, ileus, f&e imbalances, pneumonia
SCI Interventions
Vassopressors (dopamine) TEDs/SCDs (PREVENT DVT/PE) Fluid replacement Intubate/vent pulmonary hygiene Trach if long term management of airway needed
Autonomic Dysreflexia
Exaggerated autonomic response to visceral stimulation occurring in its with injuries above T6
Precipitating factors for Autonomic dysreflexia
Bladder distension, kinked foley
Bowel distension, impaction
Pressure areas, constricting clothing
Pain, spasticity
S/Sx of Autonomic Dysreflexia
- Severe Hypertension
- HA
- Bradycardia
- Sweating above level of injury
- Flushing of face/neck
- Nausea
- Nasal congestion
- Pupil dilation
Autonomic dysreflexia interventions
- Elevate HOB to lower BP
- Check for bowel impaction/bladder distension, foley patency
- evaluate skin for breakdown
- Medicate to lower BP (Hyperstat, hydalazine, resperpine)
- Atropine to increase HR
Autonomic dysreflexia meds
- Medicate to lower BP (Hyperstat, hydalazine, resperpine)
- Atropine to increase HR
Myasthenia Gravis
Autoimmune disease in which antibodies are directed against acteylcholine receptors impairing neuromuscular transmission
Myasthenic Crisis
Sudden onset of weakness, usually from UNDER MEDICATION, stress or other meds or progression of disease, manifestations include acute respiratory distress and inability speak or swallow
DRY!!!
Cholingergic Crisis
OVER MEDICATION with cholinergic or anti cholinesterase agents, manifestations include muscle weakness, GI distress (N/V/D), seating, increased salivation and bradycardia
WET!!!
Myasthenia Gravis Dx Studies
- Tensilon Test; improved muscular strength following admin of Tensilon (edrophonium) confirms Dx
- EMG
- Anti-AChR antibodies in serum
- MRI thymus gland
- Thyroid studies
Myasthenia Gravis Nursing Dx
- INEFFECTIVE BREATHING PATTERN, INEFFECTIVE AIRWAY CLEARANCE
- impaired physical mobility
- risk for aspiration
- risk for injury
- anxiety
- activity intolerance
S/S MG
Extreme muscle weakness
symmetrical muscle involvement
Ptosis and diplopia
bulbar muscle weakness; impaired chewing/swallowing
MG interventions
Plasmapheresis
Thymectomy
Hypovolemic Shock
blood VOLUME problem
Cause: hemorrhage, dehydration
Cardiogenic Shock
Blood PUMP problem
Cause: LV MI
Distributive Shock
Blood VESSEL problem
(septic, anaphylactic, neurogenic)
Causes:
neurogenic: cord injuries above T6
Anapgtlactic: type I hypersensitivity
septic: systemic inflammatory response to infection, gram neg toxins (toxic shock)
Initial Stage of Shock
Tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building
Compensatory Stage of Shock
Reversible; SNS activated by low CO, attempting to compensate for the decrease tissue perfusion
Irreversible or refractory stage
Cellular necrosis and MODs may occur, death is imminent
