ABCs First Quick History LOC Vital Signs Pupils Early or Late?
Early: restlessness, disorientation, lethargy Late: Increase BP,
pupillary changes, seizures Down and Dirty
Slide 31
Assessment GLASGOW COMA SCALE Best Eye Opening Best Verbal
Response Best Motor Response
Slide 32
Best Eye Opening Spontaneously-4 To Verbal Command-3 To Pain-2
No Response-1
Slide 33
Best Verbal Response Oriented, Converses-5 Disoriented,
Converses-4 Inappropriate words-3 Incomprehensible sounds-2 No
Response-1
Slide 34
Best Motor Response Obeys Commands-6 To Pain Localizes Pain-5
Flexion Withdrawal-4 Abnormal Flexion-3 Abnormal Extension-2 No
Response-1
Slide 35
Glasgow Coma Scale Pediatrics Verbal (2 to 5 years) Appropriate
words or -5 Inappropriate words-4 Persistent cries and/or
screams-3
Slide 36
Glasgow Coma Scale Pediatrics Verbal (0 to 23 months) Smiles or
coos appropriately-5 Cries and consolable-4 Persistent
inappropriate crying and / or screaming-3
Slide 37
Mild GCS Score 14-15 Moderate GSC Score 9-13 Severe GCS Score
3-8 Severity of Injury
Slide 38
A desk scores a 3
Slide 39
Loss of Consciousness A,E,I,O,U TIPS A Alcohol E Epilepsy I
Insulin (too much, too little) O Oxygen (too much, too little) U
Uremia or other metabolic issues T Trauma, toxicity, tumors,
thermoregulation I Infections, ischemia P Psychiatric, poisonings S
Stroke, syncope or other neurologic / cardiovascular causes
Slide 40
Babinskis Reflex Present when stroking of Planter surface of
foot causes Flexing of great toe Fanning of other toes Normally
present in children 2yo indicates problem in corticospinal tract
(nerve path spine to brain)
Slide 41
Abnormal posturing is a late sign of increasing ICP Decorticate
Abnormal flexion Decerebrate Abnormal extension
Slide 42
Meningeal Signs Nuchal rigidity Stiff neck, pain on flexion
Photophobia Positive Brudzinskis Involuntary flexion of knees/hips
when neck flexed Positive Kernigs Unable to straighten leg when hip
fully flexed in supine patient
Slide 43
Increased Intracranial Pressure
Slide 44
Intracranial Pressure Intracranial pressure reflects Brain
Cerebrospinal fluid Blood As intracranial pressure increases,
cerebral perfusion pressure decreases Leads to cerebral ischemia
and hypoxia In a hypotensive patient, even a marginally elevated
ICP can be harmful Adequacy of cerebral perfusion pressure is most
important
Slide 45
Increased Intracranial Pressure Initially -intracranial volume
increases- ICP remains stable. System becomes less compliant, or
less able to tolerate increases in volume Later, intracranial
volume conts to increase, less compliance will be unable to buffer
the increases and ICP will rise
Slide 46
Increased Intracranial Pressure Assessment Early picture of
increased intracranial pressure (IICP) LOC Loss of insight Loss of
recent memory Restless, irritable, uncooperative behavior Requires
more stimulation to get same response Speech less distinct Sudden
quietness in a very restless patient
Slide 47
Increased Intracranial Pressure Early Increasing ICP Motor
function Usually contralateral to lesion Pronator drift Loss of one
or more grades on the strength scale Increased tone
Slide 48
Increased Intracranial Pressure Early Increasing ICP Pupils
Sluggish to light response Usually unilateral Ipsilateral to lesion
Papilledema or bulging of optic discs Blurred vision
Increased Intracranial Pressure Late Increasing ICP LOC
Arousable only with deep pain Unarousable Motor function Dense
hemiparesis Abnormal flexion Abnormal extension No response
(flaccidity preliminary to death)
Slide 51
Abnormal posturing is a late sign of increasing ICP Decorticate
Abnormal flexion Decerebrate Abnormal extension
Slide 52
Increased Intracranial Pressure Decreased LOC Motor
Dysfunctions Pupillary abnormalities Impaired Reflexes Changes in
Vital Signs Irregular respirations Sign & Symptoms- Impending
Herniation
Slide 53
Increased Intracranial Pressure Late Signs Increasing ICP Vital
signs Cushings triad Very late sign of increasing ICP, last ditch
effort to perfuse brain Elevated SBP Bradycardia Widening pulse
pressure
Increased Intracranial Pressure Osmotic Agents Mannitol:
reduces ICP within 15 minutes with continued effectiveness for 2-3
hours Monitor serum osmolarity
Slide 56
Increased Intracranial Pressure Treatment of ICP Easiest to
manipulate is BP and CSF proper head alignment sedation
Surgery
Slide 57
Goal Keep SBP>90
Slide 58
Slide 59
Traumatic Brain Injury Injury to skull, brain, or both that is
of enough magnitude to interfere with normal neurological
function
Slide 60
Nearly 2 million people sustain head injuries each year
Slide 61
70,000 die prior to hospitalization
Slide 62
TBI Another 25,000 die following hospitalization
Slide 63
90,000 people will have significant permanent neurological
disabilities for the rest of their lives
Slide 64
Traumatic Brain Injury The peak age for neurotrama is 15 to 30
years of age
Slide 65
Causes of TBI
Slide 66
Slide 67
Concussion Transient impairment of neurological function caused
by a mechanical force Rapid acceleration-deceleration if repeated
can produce a permanent deterioration in intellect recent studies
suggest long term impairment even with moderateconcussion moderate
if loss of consciousness
Slide 68
Concussion Diagnosis CT scan Rule out other injury Clinical
picture History of injury
Slide 69
Concussion Interventions Assess neuro status Patient/Family
education return to facility Change in LOC Change in pupils
Projectile vomiting Seizure Inability to arouse
Slide 70
Interventions Educate patient/family Post concussion syndrome
H/A Dizziness (positional) Tinnitus Inability to concentrate
Personality change Memory disturbances
Slide 71
Interventions Educate patient/family Post concussion syndrome
Duration Days to years Social/occupational Difficulty
school/work
Slide 72
Slide 73
Diastatic Skull Fractures Fracture along suture line Often seen
in children
Slide 74
Depressed Skull Fracture A break in a cranial bone (or
"crushed" portion of skull) with depression of the bone in toward
the brain May require surgical elevation
Slide 75
Slide 76
Compound Skull Fracture A break in or loss of skin and
splintering of the bone.
Slide 77
Basilar Skull Fracture A Fracture that occurs somewhere in the
Cranial Vault
Basal Skull Fracture VIIth (Facial) Nerve Palsy Occur
immediately Occur a few days after initial injury
Slide 83
Cerebral Contusion Cerebral contusions fairly common Mostly
occur in frontal and temporal lobes Bruising of the brain tissue
without puncture of pia Petechial hemorrhages Extravasation of
fluid from vessels
Slide 84
Cerebral Contusion Distinction between contusion and traumatic
intracerebral hematoma ill defined. Contusions, can evolve into an
intracerebral hematoma
Slide 85
Cerebral Contusion Blunt force High velocity Low velocity
Slide 86
Cerebral Contusion Intervention Decrease ICP Mannitol to
decrease water content in brain Increase venous outflow Discuss
with family/patient evolution of contusion and need for monitoring
Discuss bizarre behavior- frontal lobe Assist family in
understanding a contusion to brain stem has injured awake center in
brain
Slide 87
Epidural Hematoma Located outside the dura, within the skull
Biconvex or lenticular in shape Mostly located in temporal or
temporoparietal region
Slide 88
Epidural Hematoma Result from tearing of middle meningeal
artery D/T fracture Bleeds arterial in origin Does not tamponade
50% mortality
Slide 89
Epidural Hematoma Brief loss of consciousness followed by lucid
interval then rapidly progressive deterioration Talk and die
Slide 90
Epidural Hematoma Bleeding can rapidly become mass lesion Cause
IICP Brain shift Uncal herniation
Slide 91
Subdural Hematoma More common than epidural hematomas 30% of
severe head injuries Tearing of bridging vein between cerebral
cortex and a draining venous sinus
Slide 92
Subdural Hematoma Cover entire surface of hemisphere
Slide 93
Subdural Hematoma Presentation can be Acute < 48 hours
Subacute 2 days to 3 weeks More frequent in elderly Chronic > 3
weeks
Slide 94
Subdural Hematoma Clinical findings range from headache with
nausea to comatose and flaccid
Subarachnoid Hemorrhage/Aneurysm rupture worst h/a of my life
Aneurysms result from thinning vascular wall Precipitated by
hypertensive event Straining Sex Heavy lifting
Slide 98
Subarachnoid Hemorrhage/Aneurysm rupture After rupture vessel
clamps down to prevent further bleeding Result in
Ischemia/infarction Blood in subarachnoid space is irritant
Meningeal signs
Subarachnoid Hemorrhage/Aneurysm rupture Interventions ABCs
Monitor neuro status Fluids within normal range avoid dehydration
increases hemoconcentration, increases vasospasm Monitor sodium
usually falls Normotensive BP until clipped then can be
elevated
Slide 101
Penetrating/ Perforating Injuries A foreign object penetrates
into the skull and brain
Causes of Secondary Injury Cerebral edema 1.Cerebrum 2. Skull
3. Cerebellum 4. Herniation of Brain Into Spinal Column
Slide 107
Causes of Secondary Injury Sustained hypertension
Slide 108
Causes of Secondary Injury Hypercapnia
Slide 109
Causes of Secondary Injury Seizures
Slide 110
Causes of Secondary Injury Vasospasm
Slide 111
Causes of Secondary Injury Metabolic abnormalities
(hypoglycemia)
Slide 112
Causes of Secondary Injury Ischemia (#1 cause) Normal
Ischemic
Slide 113
MAP & ICP GO HAND IN HAND MAP= Diastolic x2 Plus Systolic
Divide that by 3 ICP= The Brain The CSF The Blood
Slide 114
Cerebral Perfusion Pressure (CPP) Pressure required to maintain
adequate perfusion to cerebral tissues MAP ICP = CPP Normal: 70-100
mmHg
Slide 115
CPP < 50 mmHg Results in Ischemia
Slide 116
Spinal Cord Injuries Involve bruising or tearing of spinal cord
substance from penetrating trauma or a fracture/dislocation of
spinal column 15-35 year olds Usually due to trauma
Slide 117
Spinal Cord Injuries Mechanism of Injury Axial loading
Hyperflexion Hyperextension Injury may involve only Spinal cord
Vertebral body Both
Slide 118
Spinal Cord Injuries Damage to cord From extrinsic(bony and
soft tissue injury) From intrinsic (hemorrhage, edema, hypoxia,
biochemical changes
Slide 119
Spinal Cord Injuries Classification Complete Transection of the
cord, no preservation of motor or sensory function Incomplete Some
cord sparing
Slide 120
Spinal Cord Injuries Respiratory Complications Phrenic nerve
innervates diaphragm, exits cervical cord at C-3, C-4, C-5 if
involved diaphragm involved Compromises ability to breath
Intercostal muscles (T-1 to T-12) involved becomes difficult to
deep breath, cough
Slide 121
Neurogenic Shock Eliminates the fight or flight protective
response and permits the parasympathetic system to function
unopposed Results in vasodilation below level of the injury,
pooling of blood, decreased venous return to the heart, and
decreased cardiac output
Slide 122
Neurogenic Shock Loss of ability to sweat Below level of injury
D/T lack of innervation of sweat glands Temperature lower than
normal D/T break in connection between hypothalamus and sympathetic
nervous system Loss of body heat by passively dilated vascular bed
of skin
Slide 123
Neurogenic Shock Blood pressure may not be restored by fluids
alone In trying to normalize BP may cause fluid overload, pulmonary
edema BP best restored by judicious use of vasopressors May perfuse
adequately without normal BP
Slide 124
Intravenous Fluids Quadriplegic patients-may fail to become
tachycardic or may even become bradycardic in the presence of
shock- due to loss of cardiac sympathetic tone.
Slide 125
Intravenous Fluids Hypovolemic Shock Patient usually presents
with tachycardia Neurogenic Shock Patient usually presents with
bradycardia Overzealous fluids may cause PULMONARY EDEMA in Spinal
Cord Injury Patients If blood pressure does not improve after fluid
challenge, judicious use of vasopressors, may be indicated
Slide 126
Neurogenic Shock Orthostatic Hypotension Rapid drop in BP when
vertical position assumed. Blood supply to brain inadequate,
syncope results. (brain damage and death can result) D/T loss of
arteriole vasomotor tone below level of lesion so there is pooling
of blood in abdomen and LEs when upright. Seen in patients with
lesions above T-7
Slide 127
Spinal Cord Injuries Interventions ABCs Cervical Spine
Immobilization O2 Monitor VS, CO2 Mechanical ventilation if needed
Monitor LOC, UOP Enhance venous return to the heart Interventions
Support BP if needed Atropine if needed Methylprednisolone NG tube
Foley Attempt to have someone with patient most of the time
Slide 128
Autonomic Hyperreflexia Noxious stimuli produces sympathetic
discharge that causes reflex vasoconstriction of blood vessels in
skin and visceral bed below level of the injury Vasoconstriction of
visceral bed distends baroreceptors in the carotid sinus and aortic
arch, body attempts to lower hypertension by superficial dilation
of vessels above level of injury
Slide 129
Autonomic Hyperreflexia As spinal shock reverses, potential for
dysreflexia should be considered in patients with injuries T-6 or
above Nursing intervention prevent conditions that are know to
trigger autonomic hyperreflexia Causative noxious stimulus most
common Distended bladder d/t kinked drainage tube
Autonomic Hyperreflexia Interventions Elevate HOB Relieve
trigger mechanism Treat hypertension as needed Resources for
family/patient for self care
Slide 132
Headaches Occur when there is traction, pressure, displacement,
inflammation or dilation of pain receptors in brain or surrounding
tissues Two types: Primary No organic cause consistently identified
(migraines, cluster, tension) Secondary Organic etiology (tumor,
aneurysm, meningitis, temporal arteritis)
Slide 133
Headaches Affects up to 75% population per year 5% will seek
treatment 50 % of people with headache suffer migraine Mechanism
unknown Blood vessels that supply brain and surrounding tissue
narrow, reduced blood flow, followed by reflex vasodilatation,
swelling, and inflammation of cerebral blood vessels
Slide 134
Headaches Assessment Hx of present illness Time frame onset
(migraines early morning) Occurrence (in groups, then period of
remission) Aura (migraines with/without aura) Duration (tension 7
days, migraine 4-72 hours)
Slide 135
Headaches Pain Character and quality Intensity Therapeutic
measures implemented Success of therapeutic measures Location
Unilateral (migraine), bilateral (tension), hatband
Slide 136
Headache Symptoms with migraines Aura possible without aura
most common Nausea/vomiting Photophobia Difficulty concentrating
Visual changes May see neurodeficits in complicated migraine
Slide 137
Headache Cluster Headaches Burning, sharp, severe unilateral
orbital or temporal pain Photophobia Tearing, nasal congestion on
affected side May have lid edema, red eye on affected side. Usually
lasts < 1 hour, but may have multiple per day
Slide 138
Headaches Tension Dull, nonpulsating pain No photophobia, aura
Usually starts at occiput and moves around bilaterally to frontal
area (band like)
Slide 139
Headaches Precipitating event Emotional (stress/depression)
Metabolic (fever/menses) Flickering lights/television Alcohol
abuse/withdrawal Food Fatigue or altered sleep wake cycle
Slide 140
Headaches Physical Exam Neuro exam Edema over the sinuses
Distended, twitching scalp vessels Flushed, pale, or shiny
skin
What Is Stroke ? A stroke occurs when blood flow to the brain
is interrupted by a blocked or burst blood vessel.
Slide 146
What Is the Impact of Stroke? Stroke is the third leading cause
of death in the United States On average, someone suffers a stroke
every 53 seconds About 600,000 Americans suffer strokes each year
Every 3.3 minutes, someone dies of a stroke Stroke is the third
leading cause of death in the United States On average, someone
suffers a stroke every 53 seconds About 600,000 Americans suffer
strokes each year Every 3.3 minutes, someone dies of a stroke
Slide 147
What Is the Impact of Stroke? n Stroke is a leading cause of
serious, long-term disability n About 4 million Americans are
stroke survivors n Stroke costs the U.S. $30 to $40 billion a year
n Stroke is a leading cause of serious, long-term disability n
About 4 million Americans are stroke survivors n Stroke costs the
U.S. $30 to $40 billion a year
Slide 148
Stroke Clinical syndrome consisting of a neurological deficit
resulting from an interuption of blood flow to an area of the
brain, rapid or gradual in onset, which persists for more than 24
hours. Two types Ischemic: Thrombotic or embolic occlusion of a
cerebral artery resulting in infarction Hemorrhagic: Spontaneous
rupture of a vessel resulting in intracerebral or subarachnoid
hemorrhage
Slide 149
Slide 150
Stroke Assessment Hx present illness (time pattern)
Classifications of stroke: TIA brief, lasting seconds to hours;
< 24 hrs RIND lasting 48 hours or less, complete resolution of
deficit, reversible ischemic neuro deficit Stroke in
evolution/progressive Symptoms last >24 hrs with progressive
neurologic deterioration. Completed stroke permanent neurologic
damage
Slide 151
Stroke Medical History Diabetes Rheumatic heart disease Recent
MI CHF Migraines Hypertension A-Fib
Slide 152
Stroke Physical Exam Anterior Circulation Alteration in LOC
Motor deficit Contralateral hemiparesis, hemiplegia Sensory deficit
Contralateral
Slide 153
Stroke Physical Exam Anterior Circulation Speech deficit
Dysphasia Expressive or receptive Dominant hemisphere Visual
deficit Loss of vision in half of the visual field on same
side
Slide 154
Stroke Physical Exam Posterior Circulation (vertebral basilar)
Alteration in LOC Motor deficit more than one limb
Slide 155
Stroke Physical Exam Cranial nerve deficit Dysphonia difficulty
producing voice sounds Dysarthria difficulty in articulation
Dysphagia difficulty in swallowing
Slide 156
Stroke Physical Exam Posterior Circulation (vertebral basilar)
Visual deficits field defects, cortical blindness diplopia Loss of
coordination Ataxia
Slide 157
Stroke Ischemic Sudden, rapid onset Occurs at sleep, rest
Hemorrhagic Severe headache More gradual onset Symptoms of
increasing ICP Occurs during activity
Slide 158
Stroke Interventions Maintain airway, breathing, circulation
Monitor neuro status for change Maintain venous outflow (head
neutral position) Frequently monitor Cerebral function LOC Blood
pressure