ICP and TBI

Understanding what matters about the gray matter

Sean A Fortney, MSN, RN 17 Oct 2021

 At the completion of this
unit, the student will
have the knowledge to:
Outcome
Manage the care of a
client with a disruption in
intracranial regulation.
 At the completion of this unit, the student will
have the knowledge to:
 Explain the physiologic mechanisms that
maintain normal intracranial pressure: a)
Describe the compensatory mechanisms used to
prevent large changes in intracranial pressure
from occurring when there are changes in the
Objectives
three components within the skull- 1) brain, 2)
blood, and 3) CSF volume; b) Apply the following
concepts to the care of a client with a
neurologic injury: autoregulation, Monro-Kellie
hypothesis, and volume-pressure curve.
 Describe the common etiologies and apply to the
clinical manifestations of the client with
increased intracranial pressure.
 Determine the interprofessional and nursing
management of the client with increased
intracranial pressure.
Objectives
 Compare and contrast the intracranial pressure
monitoring devices (intraventricular catheter,
subarachnoid bolt/screw, epidural sensor,
parenchymal fiberoptic catheter) and apply to
the nursing management of the client with
increased intracranial pressure.
 Differentiate types of head injury by mechanism
of injury and clinical manifestation: a) Primary
and secondary brain injury; b) Scalp lacerations
and skull fractures (linear, depressed,
comminuted, basilar skull); c) Concussion,
contusion, coup-contrecoup, diffuse axonal injury
(DAI); d) Cerebral hematomas (epidural, subdural
[acute, subacute, chronic], intracerebral, Objectives
traumatic subarachnoid hemorrhage).
 Determine the interprofessional care and nursing
management of the client with a brain injury.
 Determine the nursing management of the client
undergoing cranial surgery.
 Sole et al., 2017: ICP and Traumatic Brain Injury,
pp. 342-371

Lewis et al., 2017: ICP, pp. 1314-1338 Lewis et

al., 2020: 1300-1323

Readings
LaCharity et al., (4th Ed pp. 82-86, 186-191, 239-
241, 282-285)

ATI RN Adult Medical-Surgical Nursing, 2016: ICP

(pp. 17-24) Head Injury (pp. 75-80) (2019: 81-
86)
Today we will cover

 The Brain
 Review of cells, functions, and limitations
 Cerebral blood flow
 Overall Anatomy
 Nursing assessment of mental status
 Intracranial Pressure and increased ICP
 Causes, treatments, monitoring, medications, nursing assessments, interventions
 Traumatic Brain Injury
 Types, classifications, monitoring, medications, nursing assessments, interventions
 The Types of Cells,
Review:
The Neuron (nerve cell)

 Passes the information along

(transmitter)
 Each one is specific to its function
 Dendrites, axon, synaptic knobs,
neurotransmitters into synaptic space
 Neurotransmitters bind, allowing for
depolarization of the next cell
 The neurotransmitter received is usually
the neurotransmitter given out
 CNS cells are surrounded by
oligodendrocytes for myelin sheathing
 PNS have Schwann cells
The Types of Cells a Review
the Neuroglial (glia)
 5-10x as many as neurons and support the neurons of the CNS
 Are the cause of gliomas
 4 types each with their own job
 Microglia – phagocytic when damage occurs to nervous tissue
 Astrocytes – transporters of food/waste/gases with blood/brain/CSF, creates scar
tissue when needed, creates the blood/brain barrier
 Oligodendrocytes – myelin formation
 Ependymal – glial tissue that forms the lining of the ventricles, central canal of the
spinal column and aid in CSF production
What can make the Neuron function
(and dysfunction)
 Acetylcholine
 Norepinephrine
 Dopamine
 Serotonin
 Glutamate
 Gamma-aminobutyric acid (GABA)
 Substance P
 Endorphins
Cerebral Circulation

 How much
 The brain receives 750ml of blood per minute (roughly 15-20% of resting CO)
 Why
 Zero energy stores and requires aerobic metabolism
 How
 2 major pairs of arteries: the carotids and the vertebrals
 Common carotids: left from the aortic arch, right from innominate artery
 Carotids: then branch to external and internal carotids
 Internal carotids: divides into anterior cerebral and middle cerebral artery (MCA)
Cerebral Circulation
-Continued
 How continued
 Anterior cerebral artery and branches supply medial motor cortex and frontal lobes
 MCA is primary blood supply for frontal, temporal, and parietal lobes
 Nearly 90% of all strokes are from the MCA (more next week)
 Vertebral arteries
 from the subclavian arteries and then through the foramen magnum.
 supply upper spinal cord, medulla, and cerebellum
 Join together at the pons to form the basilar artery
 Basilar arteries
 branch into the cerebellum, medulla, pons, and internal ear
 Bifurcates and becomes the posterior cerebral arteries
Cerebral Circulation
-Continued
 How continued
 Posterior cerebral arteries supply medial portions of the occipital and inferior
temporal lobes
 The two systems connect at the base of the brain creating the cerebral arterial
circle (of Willis)
 Posterior communicating to internal carotid to posterior cerebral, and anterior
communicating to anterior cerebral
 Cerebral veins
 have no muscle layer and no valves and flow into the venous sinuses within the cranium
into the jugular vein and eventually superior vena cava
 Play a role in CSF absorption and are more like the ventricular system than the arterial
one
Cerebral Metabolism

 Glucose!!!!!
 Any stores in the brain? Nope! None!
 BG <70 mg/dL can lead to confusion, lower can cause seizures
 BG <20 mg/dL cellular damage
Cerebral Blood Flow

 If there isn’t sufficient oxygen, the brain attempts to switch from aerobic to
anaerobic.
 Anaerobic makes extracellular fluid uptake into cells, causing edema then the
extracellular space becomes acidotic from lactic acid
 Electrical function slows, so, neurological deficits show
 Neurons permanently die beginning at 5 minutes (no regeneration)
 Autoregulation attempts to help
 If MAP low, cerebral arteries dilate
 If MAP high, cerebral arteries constrict
 Cerebral vessels also take signals from PaCO2*, PaO2, and H+ ions
Cerebral Blood Flow
-Continued
 PaCO2
 If it is >45mmHg, cerebral vessels dilate
 >35mmHg, cerebral vessels constrict
 PaO2
 <50mmHg, cerebral vessels dilate to increase blood flow
 H+ ions
 When increased, further dilation will occur to remove acidic products
The Blood-Brain Barrier System

 In a normal system
 Water, glucose, oxygen, and carbon dioxide can cross easily
 Large molecules cannot
 Chemical dissociation, lipid solubility, protein-binding potential help make the
decision for other things
 What can affect this system
 Infections
 Tumors
 Other disease states
Ventricles and
Cerebral Spinal Fluid (CSF)
 Total of 4 Ventricles
 2 lateral
 3rd ventricle at the foreman of Monro
 4th ventricle at mid cerebellar
 The lining from ependymal cells create the choroid plexus which produce CSF
 CSF
 Created at roughly 20ml/hr or roughly 500ml/day
 Roughly 150ml sit in the ventricles and subarachnoid space
 Circulates through the ventricles and then reabsorbed by the venous sinuses via the
arachnoid villi
The Meninges

 Dura mater
 Outermost against inside of skull
 Innermost produces prominent folds creating the internal cranial cavity subdivisions
 Arachnoid mater
 Avascular level loosely covering brain/spine
 Pia mater
 Directly on the brain, very vascular (less so in spine)
Breakdown of the Brain
(The Encephalon)
 Cerebrum
 Right and Left hemispheres
 Hemispheres connected by the corpus callosum
 Left hemisphere language hand movements
 Right hemisphere perception, vision
 Gyri are for increasing surface area
 Outer, cerebral cortex (just 6 cells in depth), gray matter
 Inner, myelinated axons, white matter, for association and projection
 Fissure/Sulcus separates one area from another
Breakdown of the Brain
(The Encephalon)
 Cerebrum continued
 Basal ganglia
 Diencephalon
 Connects brain stem to midbrain and cerebrum
 Thalamus
 The largest and handles every sensation but smell
 Emotions, complex reflexes, arousal/alertness
 Hypothalamus
 Regulatory system for the autonomic nervous system
 Temperature control, water balance, thirst/hunger, sleep/wake cycle, circadian rhythms, sexual
activity, cardiovascular regulation
 Subthalamus, epithalamus
Breakdown of the Brain
(The Encephalon)
 Brainstem – handles vital functions
 Midbrain (mesencephalon)
 CN III (oculomotor) & CN IV (trochlear)
 Relays information between cerebrum and lower brainstem
 Auditory and visual reflexes
 Pons
 CN V (trigeminal), CN VI (abducens), CN VII (facial), & CN VIII (vestibulocochlear)
 Between this area, and the medulla, is the respiratory center
 Medulla
 CN IX (glossopharyngeal), CN X (vagus), CN XI (accessory), CN XII (hypoglossal)
 Respiratory center, rate/strength of pulse, vasomotor activity
 Reflex reactions which include sneezing, swallowing, coughing, and vomiting
Breakdown of the Brain
(The Encephalon)
 Cerebellum
 Connected by 3 peduncles
 Receives info from the spinal cord and brainstem
 Cerebellar cortex responsible for equilibrium, fine movement, muscle tone,
balance, and coordination
Breakdown of the Brain
-What Happens Where
 Frontal Lobes
 Conscious thought, abstract thinking, judgment, contralateral voluntary movement
of the body,
 Prefrontal – affect, memory, concentration, expression of language
 Parietal Lobes
 Processing, association, interpretation of sensory input (contralateral body side)
 Temporal Lobes
 Processing, association, interpretation of auditory input, reception of language
 Medial portion memory and social behavior
Breakdown of the Brain
-What Happens Where
 Occipital Lobes
 Visual processing and interpretation
 Basal ganglia
 Fine body movement/motor control
Specialized Systems in the
Central Nervous System
 Limbic system
 Primitive control of emotional responses and arousal
 Amygdala – reward and fear
 Hippocampus – long-term memory
 Cingulate gyrus – attention and cognition
 Reticular activating system (RAS) arousal, sleep-wake cycle, selective attention.
perceptual awareness (so what happens when it is impaired?)
Assessment of Mental Status

 GCS – for consciousness and cognition

 The new one: full outline of unresponsiveness (FOUR)
 Eye, motor, breathing pattern, brainstem reflexes (0-16)
 Language – fluency, spontaneity, word-finding
 Memory – short and long
 CN function
 Motor function
 Reflexes
 Sensory function
 Client history, including comorbidities and pain
 Hourly should at least include GCS, focal motor, pupils, some CN
functions/reflexes, vital signs
Break Time
Intracranial Pressure
(ICP)
 3 things are in the intracranial vault
 Blood, Brain, CSF
 All are noncompressible
 The pressure this creates within the cranial vault is called ICP
 Normal ICP is 0-15mmHg
 CPP = MAP - ICP
 The Monro-Kellie doctrine – if one or more increases, the other(s) must
decrease (to make room), this is called compliance
 Blood to the venous sinuses, CSF to the subarachnoid space
Increased ICP

 Once compliance is exhausted it

takes a minimal shift in volume to
create a major shift in ICP
 As ICP goes up, CBF goes down
 Hypoxia results, acidosis comes into
play, cerebral blood vessels dilate to
compensate, ICP goes up!
 Any pressure >=20mmHg for >5
minutes can become life
threatening.
 Herniation is shifting of high
pressure to a lower one
 Increased ICP = brain injury & stroke
Where Does the Brain Go During
Herniation?
 Cingulate – (mass effect)
 One side to the other, no new symptoms possible but may impede CBF
 Central
 Downward shifting of the hemispheres, basal ganglia, and diencephalon through
the tentorial notch (begins to compress the brainstem)
 Early: decrease LOC, weakness, Cheyne-Stokes respirations, small reactive pupils
 Late: Coma, pupils fixed/dilated, abnormal posturing (decorticate to decerebrate),
unstable vitals leading to arrest
 Transcalvarial (external herniation)
Where Does the Brain Go During
Herniation?
 Uncal
 Unilateral lesion forcing uncus of temporal lobe to displace through tentorial notch
compressing midbrain – symptoms can progress rapidly
 Early: decreased LOC, increased tone, Positive Babinski reflex, Cheyne-Stokes respiration
(progressing to central neurogenic hyperventilation), ipsilateral dilated pupil, weakness
 Late: Pupils dilated/fixed, paralyzed eye movement (doll’s eyes), contralateral
hemiplegia, posturing (decorticate to decerebrate), unstable vital signs leading to arrest
 Cerebellar tonsil
 Cerebellar tonsils herniate through the foramen magnum, compressing pons and
medulla
Pictorial Representation of Herniations

 1 Uncal
 2 Central
 3 Cingulate
 4 Transcalvarial
 5 Upward herniation of Cerebellum
 6 Cerebellar tonsil
Causes of High ICP
Increased Cerebrospinal Fluid
 Hydrocephalus
 Block the flow
 SAH, meningitis, encephalitis
 slow the reabsorption
 SAH, meningitis, encephalitis
 increased production
Causes of High ICP
Increased Brain Volume
 Cerebral Edema is the main cause
 Increased water content
 Cytotoxic edema
 Intracellular swelling of neurons
 hypoxemia (stroke, arrest)
 In hypoxemia, cellular ATP is insufficient, sodium/potassium pump fails, sodium, chloride and
water enter while potassium leaves
 hypoosmolality (water intoxication, hyponatremia)
 Vasogenic edema
 Increased fluid in the extracellular space due to increased capillary permeability
 Brain injuries, brain tumors, meningitis, abscesses
Causes of High ICP
Increased CBF
 Obstruction of venous outflow
 Venous problems: head positioning (hyperflexion/extension, rotation), ETT or trach
securement, tumors/abscesses compressing the venous system
 Intrathoracic or intrabdominal problems: coughing, vomiting, posturing, Valsalva
maneuver, hip flexion, isometric exercise, straining for expelling, PEEP
 Increased metabolic demand
 Fever, physical activity, pain, shivering, seizures, even REM sleep
 Normal response to decreased cerebral oxygenation
 Obstructed airway, hypoventilation, even ETT suctioning
 Loss of autoregulation
 Head injury, HTN – these lead to hyperemia
Monitoring ICP
-Invasive
 Used with a GCS of 3-8 when the reason is due to severe brain insult
 Used to watch responses to therapy and interventions or to add information
to the exam
 The name of the probe is defined by where it goes in the brain
 Epidural
 Subdural
 Subarachnoid*
 Intraparenchymal
 Ventricular*
Ventriculostomy
(External Ventricular Drain [EVD])
 The gold standard
 The catheter is directly in the CSF (lateral ventricle of unaffected side)
 Allows for drainage of CSF or blood (even sampling and instillation)
 Connected to a drainage system
 Good waveform, accurate reading
 Can lead to infection (2-5%), CSF leak, excessive CSF drainage, bleeding,
longer insertion time, going through living tissue
EVD and drainage system

 Let’s look at the device and discuss the procedure

 NO PRESSURE BAG/LINE
 Preservative free saline only
 Fluid filled system most common used
 Zero and keep at the foramen of Monro
 Turn stopcock off to drain for ICP measurements
 Turn stopcock off to drain/readings for repositioning, suctioning, cough,
agitation, etc.
Subarachnoid Screw or Bolt

 Can monitor ICP

 Cannot drain or instill
 Does not penetrate the brain
 May lead to a CSF leak, poor waveform, easily clotted catheter
Other Monitoring Methods

 Epidural
 Least invasive, less chance of bleed or hemorrhage, less reliable and an indirect
measure of ICP, good for those at high risk of infection
 Subdural
 So infrequent, not even discussed
 Intraparenchymal
 Goes into brain tissue
 Quick, reliable, fragile, expensive, no CSF drainage possible
The Types of ICP Monitoring Devices
  P1 – Percussion (cardiac systole)
 P2 – Tidal (intracranial brain bulk)
 P3 – Dicrotic (cardiac diastole)
 Other waves may exist
 If P2 is higher than P1, there is non-
The waveform compliance.
 Always zero your device, note
placement of transducer, and
waveform upon arrival
Cerebral Oxygenation Monitoring
Jugular oxygen saturation (SjO2)
 Similar tech to SvO2
 Fiberoptic catheter placed into jugular venous bulb via internal jugular
 verified by X-ray
 Reading should be between 60-70%
 Readings <50% represent cerebral ischemia
 This is a global reading of the brain
Cerebral Oxygenation Monitoring
Other Methods
 Partial pressure of the oxygen within brain tissue (PbtO2)
 Probe directly into the white matter
 Go into the injury to see its oxygenation, unaffected side for global oxygenation
 >20mmHg is good… but maybe not?
Other Monitoring

 SpO2
 Hemodynamics
 End-tidal CO2
 Occasional ABGs
 Possible EEG to correlate with ICP or for sedation/NBM
 BIS
 Micro dialysis (never seen it)
Diagnostic Testing

 ABGs
 CBCs (H&H, plt)
 Coags (brain injury can induce coagulopathy, and poor coagulopathy could
lead to bleeds)
 Electrolytes, liver function, BUN, Cr, serum osmolarity
 CT, MRI, Transcutaneous dopplers (vasospasm)
 EEG
 Evoked potential monitoring (never seen it)
Managing a High ICP

 The Goal: Keep ICP <20mmHg while keeping CPP >70mmHg

 Keep ICP from going up
 If ICP goes up, treat then find and correct the cause
 Maintain CPP, airway, ventilation and oxygenation, decrease the metabolic
need of the injured brain
Nursing Interventions

 HOB 30degrees and neck neutral (unless MAP low)

 Continue to turn client
 Suction only when needed and preoxygenate (10 second passes x2)
 Allow only a few minutes of grouped activity at at time for a return to
baseline ICP
 Family presence but only with low stimulation (calm, not discussing negatives
of the situation)
Medical Interventions

 Adequate oxygenation/ventilation (perhaps even hyperventilation)

 PaO2 >80mmHg, good H&H
 Hypocapnia for cerebral vessel constriction (short term only or refractory
conditions) – long term would require brain O 2 monitoring methods
 Osmotic and loop diuretics
 Osmotic: mannitol, hypertonic saline pulling extracellular fluid to the plasma, can
result in hypotension, electrolyte disturbances, rebound increased ICP,
hyperosmolality
 Loop: removes sodium and water from brain cells, slows CSF production
 Euvolemic fluid administration
 Use NS, avoid hypotonic solutions (edema), strict I&O, watch electrolytes
 Serum osmolarity to remain <320 mOsm/L
Medical Interventions
Proper B/P maintenance

 MAP 70mmHg - 90mmHg but balanced with ICP for a CPP of >70mmHg
 However, SBP >160 = increased microvascular pressure possibly causing
increased cerebral edema
 Labetalol helps with the catecholamine release in neuro injuries. Nicardipine
is quick acting and works well
 Antihypertensives to avoid are nitroprusside, nitroglycerin, some Ca+ blockers
(verapamil and nifedipine) cause vasodilation (including cerebral vasodilation)
causing increased CBF causing higher ICP despite the lower SBP
Medical Interventions
Reduction of Metabolic Demands

 Temperature control
 Normothermia, induced hypothermia (34-35degrees for 24 to 72 hours) via cooling
blankets, skin pads, or cooling catheters
 Sedation
 Propofol reduces cerebral metabolism and ICP, Benzos do not affect CBF or ICP
 Morphine and fentanyl for analgesia and sedation
 Seizure prophylaxis
 NMB
 Usually used when other treatments fail
 Barbiturate therapy
 Usually used when ICP remains refractory to treatment
Medical Interventions
Corticosteroids
 Only for cerebral edema with brain tumors and meningitis
Some Medication Choices

 Diuretics
 Mannitol, hypertonic saline, furosemide
 Corticosteroids
 Dexamethasone, methylprednisolone
 Antihypertensives
 Labetalol, nicardipine, enalapril
 Antiseizure
 Phenytoin, Fosphenytoin, levetiracetam, adjunct with diazepam
Some Medication Choices

 Sedatives
 Ativan, propofol, adjunct diazepam
 NMB
 None specific listed for neuro injuries
 Barbiturate therapy
 Pentobarbital (NOT phenobarbital)
 Vasospasm control
 Nimodipine
 This is not normally used with traumatic subarachnoid hemorrhage
Surgical Interventions for High ICP

 Remove the mass or lesion

 Remove the hematoma
 Decompressive hemicraniectomy
Break Time

 When you come back, please be in your groups for activities after last bit of
lecture
Traumatic Brain Injury (TBI)

 Open or closed (no break in the scalp is closed)

 Most common type is acceleration/deceleration with or without rotation
 Genetics can play a role in injury and recovery
 If you can hurt your head in the injury, you can hurt your neck, more on that
later
 Major types of injuries
 Scalp lacerations – if you have one, you probably have a skull fracture (depressed)
 Skull fractures
 Brain injuries both primary and secondary
TBI
Skull Fractures - Linear

 Most common
 Usually not a problem unless moves across a complicated
area (orbit, sinus, vessels)
 If the fracture extends beyond the point of contact, client
is admitted for possible head bleed and observation
 If at base of skull, it is called a basilar fracture
 Difficult to see on X-ray look for battle sign/racoon
eyes
 Dural tears can occur with this leading to infection
and meningitis
 Dural tear can lead to rhinorrhea and otorrhea with
CSF, let it flow
 Basal fracture possible? Avoid the nose for tubes of
any kind
TBI
Skull Fractures
 Depressed
 A portion of the skull is below the rest, this can cause Dural bruising and tearing
 The brain may be in direct communication with the environment (meningitis)
 The brain parenchyma held beneath the bone will show deficits and possible focal
seizures
 Comminuted
 This is a combination of multiple linear fractures around a depressed fracture at
the point of injury
 “Eggshell” fracture
TBI
Skull Fractures
 The skull has compressive strength, bending in at point of impact, bending
out at point of vertex
 Fracture lines move toward the base of the skull
TBI Classifications

 Primary or Secondary
 Primary Brain Injury – direct injury due to an impact
 Coup, contrecoup
 Stretching/shear/rotation/tearing
 Types include concussions, contusions, diffuse axonal injury, penetrating injury, and
hematomas (epidural, subdural, intracerebral)
 Secondary Brain Injury
 Due to the release of cytokines (from macrophages) as the inflammatory response
to the primary injury causing increased vascular permeability of the vessel walls
(resulting in vasogenic cerebral edema) and other reactive events
TBI
Primary Brain Injury
 Concussion
 Results in a temporary failure of impulse conduction with generally mild deficits
that are often reversible, this may include loss of consciousness
 Contusion
 Coup/contrecoup injury causing bruising and bleeding into the brain tissue, deficit
will depend on location and size, contrecoup can be larger than the original injury
 Diffuse axonal injury
 Global brain injury with a poor prognosis due to white matter (axon) injury
secondary to rotational and shearing forces
TBI Primary Brain Injury
Penetrating Injury
 Low or high velocity intrusion (gunshot, knife, nail, etc.)
 Low velocity is contained to the tract of the injury watch for bleeding &
infection
 High velocity extensive damage due to shockwaves and ruptured skull &
penetrating item
TBI Primary Brain Injury
Hematomas
 Can be life threatening if acute
 Epidural
 Inside the skull, outside the dura
 Often a linear fracture of the temporal bone
 Loss of consciousness, lucid period, decreasing LOC within 48 hours with ipsilateral
pupil fixation/dilation and contralateral body deficits
 Subdural
 Torn surface vein of the cerebral cortex
 Acute – <48 hours after injury due to a cortical or brainstem injury and causes a
mass effect, increased survivability if surgery occurs within 4 hours
TBI Primary Brain Injury
Hematomas
 Subdural continued
 Subacute - 48hrs to 2 weeks after injury slow growing
 Chronic – due to low velocity impact occurring from 2 weeks to several months, this
is often missed as symptoms are subtle to change and often occur in the elderly,
alcoholics, and those on blood thinners
 Intracerebral
 A mass lesion as it occurs within the brain tissue, can happen anywhere within the
brain due to any type penetrating injury including depressed skull fractures or as a
result of the extension of a contusion
 S&S depend on size and location
TBI
Secondary Brain Injury
 Due to the release of cytokines (from macrophages) as the inflammatory
response to the primary injury causing increased vascular permeability of the
vessel walls (resulting in vasogenic cerebral edema)
 Free oxygen radicals disrupt cellular membranes and cellular metabolism
causing neuron damage
 Decreased cerebral perfusion from hypoxia, infection, fluid/electrolyte
imbalances, and more add to this
 This extends the damage, increases the deficit, and lowers recovery
 We must manage the client well to avoid this
 The vicious cycle: loss of autoregulation leads to too much blood in the brain
cavity or ischemia which leads to increased ICP which leads to more ischemia
and therefore cellular failure or cellular infarction leading to cell death
Assessment of the Client with TBI

 GCS
 Neuro exam with specific attention to area of deficit
 Airway/oxygenation/ventilation
 Respiratory Patterns
 ICP, CPP, hemodynamics
 Same labs and diagnostics as those with increased ICP
Medical Management of TBI

 Maintain Airway
 Provide Oxygen as needed
 Maintain cerebral perfusion
 PREVENT SECONDARY BRAIN INJURY
 Nutritional support
 TBI causes hypermetabolism, excess nitrogen loss, increased catabolism
 Possible induced hypothermia
 Lowers metabolic needs
 Lowers ICP
 Raises risks with dysrhythmias, electrolyte imbalances, coagulopathies, acidosis,
shivering
Surgical Interventions for TBI

 Based on type of TBI

 Depressed skull fractures, elevate the skull, remove the outlying pieces
 Acute subdural hematoma, use burr holes to evacuate
 Epidural hematoma, craniotomy for evacuation
 Penetrating wound, craniotomy to explore/repair/retrieve
 These clients are at high risk for infection and abscesses
 Afterwards, watch ICP, CPP, MAP, airway/oxygenation/ventilation,
fluids/electrolytes, nutrition, immobility, risk of infection, dural leaks
 If a leak occurs, a lumbar drain or ventriculostomy may be necessary for
several days
A Few Nursing Diagnoses
Increased ICP and TBI
 Decreased intracranial adaptive capacity
 Ineffective cerebral tissue perfusion
 Imbalanced fluid volume/electrolyte status
 Altered thought processes
 Additional diagnoses will include impaired swallowing, impaired sensation,
hyperthermia, pain, decreased CO, risk for infection, imbalances in nutrition,
impaired communication
That’s the Basic TBI

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