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1. NATIONAL INSTITUTE OF MENTAL HEALTH AND NEUROSCIENCES (INI) – BENGALURU
SUBJECT: NEUROSCIENCE NURSING-II
UNIT- VIII Traumatic conditions.
TOPIC: Cranio cerebral injuries.
SUBMITTED TO: SUBMITTED BY:
DR. GOPI CHANDRAN.L, MRS. KRISHNAMMAL.T,
ASSISTANT PROFESSOR, II YR M.SC NS NSG,
DEPT OF NURSING DEPT. OF NURSING,
NIMHANS. NIMHANS.

2. CRANIOCEREBRAL TRAUMA
Definition:
Injury to the skull, brain, or both that is of sufficient magnitude to interfere with
normal function and to require treatment.

3. Craniocerebral trauma can be classified according to location:

4. Clinical severity of TBI may be classified based on the Glasgow Coma Scale (GCS) after initial resuscitation:
Mild TBI (GCS 13 – 15), Moderate (GCS 9 – 12), or Severe (GCS 3 – 8)

5. ETIOLOGY
The principle causes of head injury include
 Road traffic accidents,
 Falls, assaults, and injuries occurring at work, in the home,
and
 During sporting activities.
 Alcohol may be involved in up to 65% of adult head injuries.

6. INCIDENCE:
• The incidence of penetrating head trauma remains low.
• Assaults (30 – 50%) and falls (22 – 43%) are the most common
cause of mild head injury.
• Road traffic accidents are responsible for a large proportion of
moderate–severe head injuries. India has one of the highest TBI
burdens due to road traffic accidents (RTAs), with 60% of head
injuries being attributable to RTA and more than 150,000 lives
being lost annually due to traumatic brain injury (TBI).
(Veerappan VR, Nagendra B, Thalluri P, Manda VS, Rao RN,
Pattisapu JV. Reducing the Neurotrauma Burden in India—A
National Mobilization. World Neurosurgery. 2022 Sep
1;165:106-13.)

7. PATHOPHYSIOLOGY
There are two main stages in the development of brain damage after
TBI:
Primary injury and Secondary injury.
The primary injury comes through direct contact to the head and
brain as an immediate result of the initial insult at the moment of
injury. The cerebral injury may be focal (contusion or laceration) or
diffuse (concussion or diffuse axonal injury).

8. PRIMARY BRAIN INJURY:
 Impact loading involves direct contact of an object to the head, which
results in skull deformation and/or fractures.
 Impulse loading results when another part of the body has direct contact
to the object and the head moves as a consequence. This type of mechanical
load does not cause skull fractures.
 Static loading is caused by a compressive force to the head, which may
result in skull compression and fracture. Head motions caused by these
mechanical forces result in contact phenomena injuries and head motions of
accelerations and deceleration.

12. SECONDARY BRAIN INJURY:
Secondary injury is a delayed, physiologic response to the
primary injury.
After the primary insult
Neuropathological changes occur
[activation of biochemical, metabolic,
and inflammatory cascades]
Ischemia, cerebral edema, inflammation, and
neuronal defect.

13. PRIMARY INJURY: DIAGNOSIS AND MANAGEMENT
Scalp Lacerations
Abrasion: the top layer of the scalp is scraped away-slight bleeding- Dressing
needed
Contusion: the scalp is bruised with possible effusion of blood into the
subcutaneous layer without a break in the integrity of the skin; there is no specific
treatment.
Laceration: the scalp is torn and may bleed profusely; suturing may be necessary
Subgaleal hematoma: a hematoma in the subgaleal layer of the scalp occurs and
will usually absorb on its own.

16. Skull Fracture
Linear: a singular fracture line occurring to the skull
Comminuted: the skull is splintered or shattered into pieces
Depressed: a fracture of the skull in which a fragment is depressed; the scalp
and/or dura may or may not be torn
Open depressed fracture: also known as compound skull fracture; is an
opening of the skull as a result of comminuted depressed skull fractures and
tearing of the dura mater and the scalp.
Basal skull fracture: often arises from extension of a linear fracture into the
base of the skull.

18. Diagnosis:
o CT -skull fracture
o MRI- associated brain injury
o Common findings of anterior fossa fractures (fractures of the paranasal sinuses) include the
following:
• Rhinorrhea (drainage of CSF, blood, or both from the nose)
• Subconjunctival hemorrhage of the eye
• Periorbital ecchymosis (raccoon’s eyes)
o With middle fossa fractures (fractures associated with fracture of the temporal petrous bone),
common findings include
• Otorrhea (drainage of CSF, blood, or both from the ear)
• Hemotympanum (blood behind the tympanic membrane)
• Battle’s sign (ecchymosis over mastoid bone that develops 12 to 24 hours after injury)
• Conductive hearing loss (may be associated with signs of vestibular dysfunction, such as
vertigo, nausea, and nystagmus)
• Possibly facial nerve palsy (Bell’s palsy) that appears 5 to 7 days after injury.

21. Treatment:
 Treatment of skull fractures depends on the type of fracture.
 Generally, linear skull fractures -observation for underlying cerebral injury.
 A depressed skull fracture with an open scalp, skull, and dura mater requires surgery
to débride, elevate, and remove bone fragments from the wound. If the fragments are
extensive, a craniectomy may be necessary.
 To aid resolution of leakage lasting more than 4 to 5 days, a lumbar catheter for
continual drainage of CSF may be inserted. If leakage of CSF continues, a craniotomy
may be necessary to repair the tear surgically or to repair the leakage with grafts.

22. Traumatic Brain Injuries
Injuries to the brain can be focal or diffuse.
Focal Cerebral Injuries: Contusions, Lacerations, and
Hematomas
 A cerebral contusion is a bruising of the surface of the
brain (cerebral parenchyma). Contusions may occur from
blunt trauma (direct contact), a depressed skull fracture, a
penetrating wound, or an acceleration-deceleration closed
injury.
 Cerebral Lacerations. A cerebral laceration refers to a
traumatic tearing of the cerebral tissue. It is related to high
impact injuries and is treated in the same manner as a
cerebral contusion is managed.

23.  Intracranial Hemorrhage/Hematomas. Traumatic
intracranial hemorrhage is a common complication of TBI.
The major types of bleeding associated with head trauma are
 epidural hematoma (EDH),
 subdural hematoma (SDH), and
 intracerebral hematoma (ICH).
Other focal bleeding includes
 traumatic subarachnoid hemorrhage (TSAH) and
 intraventricular hemorrhage (IVH)

24. Epidural Hematoma.
• EDH, also known as an extradural hematoma, refers to bleeding into the
potential space between the inner table of the skull (inner periosteum) and
the dura mater.
• Epidural hematomas are seen most often in children older than 2 years old
and young adults because their dura is less firmly attached to the bony table
than it is in older adults.
• As the bleed expands, it gradually strips away the dura from the inner table
of the skull, and a large, ovoid mass develops, creating pressure on the
underlying brain and causing a mass effect.

25. • Clinically, the “classic” description of an EDH was that of a momentary
unconsciousness followed by a lucid period lasting for minutes to several
hours.
• Other findings include ipsilateral pupillary dilation, contralateral
hemiparesis, headache, vomiting, seizures, and hemi-hyperreflexia with a
unilateral Babinski sign. In 60% of patients, a unilateral dilated ipsilateral
pupil without loss of consciousness is found. Bradycardia and respiratory
distress are late findings. If untreated, neurological deterioration may occur
from drowsiness to lethargy and then to coma as mass effect and herniation
developed.

26. EDHs are commonly identified through CT scan of the head (without
contrast), which appears as a biconvex or lenticular high-density lesion
adjacent to the skull.
Immediate diagnosis and surgical evacuation of the hematoma are
associated with lower mortality rate. Prognosis is associated with the severity
and the duration of the brain compression caused by the EDH. Therefore, early
diagnosis and management are important.
Surgical indication includes symptomatic EDH and/or acute, greater than 1-
cm bleed.
Presence of coagulopathy associated with a hematoma should also be
identified and optimally corrected to promote hemostasis and prevent
rebleeding.

28.  Subdural Hematoma. An SDH refers to bleeding between the dura mater and
arachnoid or pial layer. Approximately 30% of patients with posttraumatic
intracranial lesions have SDHs.
 Causes:
o tearing of the bridging veins located over the convexity of the brain.
o tearing of small cortical arteries.
o cerebral contusions, and acute bleeding into chronic SDHs
 Clinical presentations are usually due to brain compression and vary according
to the location of the lesion and the interval between injury and presentation of
symptoms.
o Acute SDH.
o Subacute SDHs
o Chronic SDHs

29.  Diagnosis: CT scan of the head will reveal a crescentic
hyperdense lesion with edema/mass effect in acute SDH. Unlike
EDH, CT scan findings of acute SDH appear concave over the
brain surface and more diffuse.

30.  Management:
o Immediate surgical evacuation of the clot is recommended
for symptomatic SDHs that are greater than 1 cm in
thickness.
o Factors that affect outcome include initial Glassgow Coma
Scale (GCS) score, pupillary status, time interval between
trauma and treatment, clot size, mass effect, and presence of
other traumatic lesions.

31.  Intracerebral Hematoma.
An ICH refers to bleeding into the brain parenchyma resulting from contusions
or blood vessel injury. Approximately 16% of TBI cases are due to ICH.
Common locations are below the surface of the cortex in the basal ganglia or
white matter.
Manifestations include headache; altered mental status, which can vary from
confusion to a reduced level of consciousness or coma;

32. Diffuse Cerebral Injuries: Concussions and Diffuse Axonal Injuries
 Concussions: A cerebral concussion is defined as a transient, temporary,
neurogenic dysfunction caused by mechanical force to the brain.
 Causes: Acceleration-deceleration (with shearing stress on the reticular
formation) is the mechanism of injury usually due to a nonpenetrating injury such
as a sudden blow to the head.
 Signs and symptoms may include
o immediate unconsciousness lasting a few seconds, minutes, or hours;
o momentary loss of reflexes;
o and momentary (few seconds) and possible retrograde or antegrade amnesia (loss
of memory for events immediately before and after the injury, respectively).
o Other presentations
 Concussions are classified as mild or classic

33.  Diffuse Axonal Injury.
DAI is a primary TBI associated with acceleration-
deceleration during which shearing forces damage nerve
fibers at the moment of injury.

34.  Classifications:
Mild DAI: coma lasting 6 to 24 hours with the patient beginning to
follow commands by 24 hours. Outcome: death is uncommon, but
cognitive and neurological deficits are common.
Moderate DAI: coma lasting longer than 24 hours, but without
prominent brainstem signs. This is a common presentation (about 45% of
all patients). Outcome: incomplete recovery in those who survive.
Severe DAI: coma is prolonged and associated with prominent
brainstem signs (e.g., decortication, decerebration). This presentation is
seen in about 36% of all DAI patients. Outcome: death or severe
disability.
 Management:
The treatment is supportive care, specifically to the unconscious patient.
DAI is associated with significant disability or death whether or not there
is a coexisting traumatic lesion such as contusion or hematoma.

35. MANAGEMENT OF THE TRAUMATIC BRAIN INJURY PATIENT: THE
CONTINUUM OF CARE
Mild TBI
 (GCS =13 to 15) is a transient event in which there may be a
dazed appearance, unsteady gait, and short-term confusion after
a blow to the head.
 The patient feels well after a few minutes; most patients have
full recovery without problems. Some will have posttraumatic
amnesia and post-concussion syndrome.
 A subgroup of patients, who seem perfectly fine when seen,
develop secondary brain injury and die.
 That all patients with a mild TBI need to be observed and
monitored for evidence of deterioration is clear.

36.  Admission is warranted for patients in the following situations:
 loss of consciousness; neurological deficits; CSF leak or
drainage from the nose or ear; alcohol consumption or other
medical condition that makes assessment difficult; and absence
of a support person to monitor them for 24 to 48 hours.
 People exhibiting no significant signs and symptoms may be
sent home with a responsible person. Written instructions
should outline what signs and symptoms may develop and what
should be done if they appear

37. Moderate TBI (GCS 9 to 12)]
 It indicates that more significant brain damage has occurred
than with mild TBI.
 Patient is often initially managed as a multisystem trauma
patient with all the precautions (e.g., cervical neck injury
immobilization) outlined for severe TBI.
 After the patient has been stabilized, a CT scan should be done
as soon as possible.
 Patients with moderate TBI requires frequent neurological
monitoring and involves the same complement of management
considerations outlined for severe TBI.
 Serious postinjury deficits may develop that can affect the
person’s ability to work and function effectively.

38.  Moderate TBI patient needs to be monitored after
discharge and provided with appropriate rehabilitation
services and counseling, as needed.
 Complaints of irritability, fatigue, headache, difficulty
concentrating, dizziness, and memory problems, called
postconcussion syndrome, often arise after moderate TBI.
 Anxiety and depression are also frequently noted.
 Targeted education and supportive counseling are helpful
in assisting the patient and family to cope with
postconcussion syndrome.
 Symptoms usually subside with time but may last for
months before resolution is complete.

39. Severe Traumatic Brain Injuries
 Severe TBI refers to a brain injury that results in a GCS of 8 or
less.
 This patient population is associated with high morbidity and
mortality risks and requires intensive care.
 The first priority for the initial management for TBI patients is
complete and rapid physiologic resuscitation, which includes
airway, breathing, circulation, and disability.
 The latter was added to emphasize the significance of early
recognition and stabilization of any neurological injury.

40. PREHOSPITAL MANAGEMENT

41. EMERGENCY DEPARTMENT OR TRAUMA CENTER MANAGEMENT
Activity includes
 inserting arterial and central lines,
 inserting an indwelling urinary catheter,
 attaching monitoring equipment such as continuous electrocardiography, and
 conducting primary and secondary trauma surveys.
The history and circumstances of injury and previous treatment are verified and clarified. The
following are examples of important information to consider:
o Circumstances of injury (e.g., direct blow to head, thrown from car, fell off bar stool)
o Seat belt or helmet worn (e.g., type of seat belt: lap or shoulder)
o How patient was found (e.g., lying face down)
o Unconsciousness (immediate; lucid period)
o Documented apnoea or cyanosis and length of time
o Significant blood loss at the scene of accident.

42. Cont…..
• CT scan is the “gold standard” for diagnosis of TBI.
• Cerebral angiograms or MRI may be ordered to exclude any vascular
injury secondary to trauma such as arterial dissection, traumatic
aneurysms, arteriovenous fistula, or venous occlusions.
• ICP monitoring
The management of the TBI patient in the ED is directed at
 Resuscitation, stabilization, and establishment of a diagnosis.
 After these steps have been completed, a decision is made regarding
immediate surgical intervention for life-threatening injuries or transfer to
the intensive care unit (ICU) for medical management.

43. INTENSIVE CARE UNIT MANAGEMENT OF SEVERE TRAUMATIC BRAIN INJURY
The goals of ICU care are to
 manage intracranial hypertension,
 maintain adequate cerebral oxygen delivery to meet cerebral metabolic needs,
 prevent secondary brain injury, and
 prevent or manage potential or actual systemic problems that can contribute to morbidity and mortality.
Monitoring
Systemic Monitoring:
 Cardiac rhythm monitoring via telemetry,
 pulse oximetry for oxygen saturation,
 invasive arterial blood pressure monitoring via arterial line,
 temperature monitoring, and
 end-tidal CO2 monitoring
 Central venous pressure monitoring
 pulmonary artery flotation catheter may be placed in hemodynamically unstable patients for further monitoring
and direction in management
 Strict intake and output recording
 Regular monitoring of blood glucose, serum electrolytes, and arterial blood gases

44. Cont…..
Cerebral Monitoring:
• ICP monitoring
• Intraventricular catheter placement
Management of Intracranial Hypertension
Applying the Monro-Kellie principle, intracranial hypertension can be
therefore achieved by any of the following components:
• Decrease brain size: mannitol or hypertonic saline
• Decrease CSF: drainage
• Decrease blood: inducing vasoconstriction with hyperventilation
• Removal of the pathologic process (e.g., tumor or clot)
• Removal of a bone flap to allow expansion of the brain (craniectomy).

45. Cont………
Management of intracranial hypertension is usually done in a
stepwise approach, moving from one therapy to another only if ICP
remains uncontrolled with the present treatment.
• CSF drainage,
• sedation/analgesia, chemical paralysis,
• hyperventilation (PCO2 35 to 40 mm Hg), and
• hyperosmolar therapy with mannitol.
Other Therapeutic Measures
Other available alternative management strategies for intracranial
hypertension include
• decompressive craniectomy,
• use of hypertonic saline solution, and
• hypothermia.

46. • Seizure Management
• Multisystem Management:
Extracranial factors such as hypotension, hypoxemia, hypercapnia, hypocapnia, hyperthermia,
hyponatremia, hyperglycemia, and hypoglycemia can cause secondary brain injuries.
• Cardiovascular Management
• Respiratory Management
• Hematologic Management
• Infection Control
• Temperature Control
• Electrolyte Management
• Endocrine Management
• Autonomic Management
• Gastrointestinal Management

47. MANAGEMENT OF SEVERE TRAUMATIC BRAIN INJURY DURING THE POSTACUTE
PHASE:
• REHABILITATION

48. ASSESSMENT AND CLINICAL REASONING: KEY ROLE OF THE
NEUROSCIENCE NURSE IN PATIENT CARE
• The frequency for monitoring vital signs depends on the stability of the patient’s
condition.
• In the ICU setting, monitoring should occur at least every hour unless the patient is
physiologically unstable.
RESPIRATIONS:
• Brain injuries can result in abnormal respiratory patterns
• In general, an initial increase in intracranial pressure (ICP) results in the slowing of
respirations. If ICP continues to increase, the pattern becomes rapid and noisy until the
terminal stage, when respirations cease
• A few conditions can affect respirations:-Complications of metabolic disorders, such
as diabetic acidosis, can change respiratory patterns (Kussmaul's respirations).-
• Injuries to the cervical spine below C-4 can cause respiratory difficulty, whereas
injuries above C-4, the site of phrenic nerve innervation, can cause total arrest

49. Cont…….
BLOOD PRESSURE
• Cushing's response is an ischemic response of the body that maintains
cerebral blood flow in the presence of rising ICP
• Cushing's response includes hypertension, bradycardia, and a widening
pulse
• Cushing's triad includes hypertension, bradycardia, and an irregular
respiratory pattern; it reflects a rising ICP in which there is direct
pressure on the medullary center of the brainstem. It is often seen in the
terminal stage and is associated with irreversible brainstem damage.
PULSE:
• Brodycordia is associated with increasing ICP or cervical injury.
• Tachycardia is associated with the following-Occult (nonneurological)
hemorrhage or hypovolemic shock -An autonomic response to injury
of the hypothalamus or its connections-A terminal event in severe brain
injury

50. TEMPERATURE:
• Hypothermia can occur as a result of hypothalamic injury, also seen
early in cervical cord injuries.
• Hyperthermia in the brain-injured patient can be associated with
direct injury to the hypothalamus or petechial bleeding into the
hypothalamus or pons.
• Hyperthermia must be controlled because it increases the metabolic
rate of all body cells, including those in the brain. Oxygen
consumption rises approximately 10% for every 1°C rise in
temperature.
• A rise from 37°C (98.6°F) to 40.5°C (105°F) results in a 35 increase
in oxygen consumption of brain.

51. Neurological Signs
• The frequency with which a serial neurological assessment is conducted
depends on the patient’s condition and degree of stability.
• In the unstable patient, neurological signs may be monitored as
frequently as every 5 to 15 minutes. After the patient has been well
stabilized, monitoring every 2 to 4 hours may be safe and appropriate.
• Level of consciousness and cognition (if responding verbally); if
comatose, GCS is used.
• Brainstem Reflexes:
 Size, shape, and reaction of pupils to light (asymmetry seen with a
focal lesion)
 With lateral transtentorial herniation caused by localized cerebral
edema (peaks about 72 hours after injury) or a focal lesion, one pupil
will become dilated and progressively unresponsive to light.

52.  An oval or ovoid pupil is also an early sign of transtentorial herniation.
Immediate intervention may be necessary to prevent herniation and
irreversible neurological deterioration.
 The corneal and gag reflexes can be assessed easily at the bedside.
 The absence of either of these reflexes is a poor prognostic sign. Special
protective eye care and lubrication should be applied if the corneal
reflex is absent.
 Symmetry of the facial nerve can be checked by inserting a cotton-
tipped applicator first in one nostril and then the other.
 Without a gag reflex, the patient is at high risk for aspiration
pneumonia.
 The eyes can be checked for doll’s eye reflex (oculocephalic reflex)

53. Motor Function:
• Observe the patient for spontaneous movement. Asymmetry of
movement or lateralization suggests a focal mass lesion on one side of
the brain.
• Decortication (flexor) or decerebration (extensor) posturing is observed
in comatose patients who have suffered severe TBI.
• Additionally, bilateral or unilateral flaccidity may be associated with
spinal injuries.

54. NURSING MANAGEMENT OF TRAUMATIC BRAIN INJURY
• A critical management and care focus for TBI patients is prevention of
secondary brain injury by optimizing cerebral perfusion, early
recognition of complications, and management of multisystem
problems. To achieve optimal outcomes for the patient, a collaborative.
• Nursing measures to treat and/or prevent ICP elevation include proper
positioning, elevation of the head of bed at 30 degrees, and prevention
of jugular venous outflow obstruction by keeping the head in midline
position.
• Cervical collar and endotracheal tubes must also be checked for
tightness around the neck.
• Minimizing external stimulation is important.
• Use pharmacologic orders for sedation and analgesia as needed when
providing potentially uncomfortable procedures such as wound care.

55. • Proper timing of the necessary procedures to allow for rest periods is also
helpful. If the patient has an external ventricular drain, it may be
necessary to open the drain to allow for CSF drainage to treat ICP
elevations, according to unit protocol.
• Position the patient on the side to facilitate drainage of secretions and
prevent aspiration, if not intubated.
• Maintaining a patent airway, the common pathway to the respiratory
system, is another top priority in TBI management.
• Preoxygenate with 100% oxygen before suctioning (with physician’s
approval). • Limit the catheter insertion to 10 seconds or less to prevent an
increase of CO2.
• If a tracheostomy is present, provide tracheostomy care frequently,
according to unit protocol, to prevent crusting and build-up of secretions
that can obstruct the airway.
• Do not hyperextend or hyperflex the neck, because such maneuvers create
a partial obstruction of the airway.

56. NURSING MANAGEMENT FOR SPECIAL PROBLEMS
Basal Skull Fractures
Signs and symptoms may include
 ecchymosis of the mastoid process (Battle’s sign),
 periorbital hemorrhage (raccoon’s eyes) and ecchymosis,
 blood behind the eardrum (hemotympanum),
 decreased hearing,
 drainage from the nose (rhinorrhea) or ear (otorrhea), and
 postnasal drainage (postnasal drip)

57. Nursing management addresses the risk of meningitis through the following strategies:
 Never suction through the nose if there is question of a basal skull fracture; the catheter
could slip into the dural tear and become a source of contamination within the intracranial
cavity.
 In a conscious patient, caution against blowing the nose; this act could introduce
microorganisms into the meninges or brain through a dural tear.
 Do not introduce any foreign body into the orifice (nares or ear) or irrigate the area; sterile
cotton or other absorbent material should be placed loosely around the orifice and changed
frequently.
 If there is any question whether the drainage is CSF, laboratory analysis of a test tube
specimen for chloride concen tration is helpful. CSF’s chloride concentration is greater
than that of serum. A characteristic stain with a dark center and a lighter outer area (halo
sign) is often seen. Most CSF leaks heal spontaneously within days. In rare instances,
surgery is necessary to find and patch the tear.
 Use of prophylactic antibiotics for basal skull fractures is controversial. A basal skull
fracture can be very serious if rapidly developing local edema is close to vital brainstem
structures. It can lead to life-threatening respiratory problems, including respiratory arrest.
 Nursing management includes monitoring for deterioration in vital or neurological signs as
well as for signs of meningeal irritation.

58. Nursing Interventions:
1. Nsg Diagnosis: Ineffective Cerebral Tissue Perfusion related to (hemorrhage, skull fractures cerebral edema
(localized or generalized response to injury), decreased systemic blood pressure, hypoxia) as evidenced by
mental status changes, decreased LOC, pupillary changes, changes in motor response, difficulty swallowing
or speaking.
Goals: The patient will maintain an expected level of consciousness, motor response, sensory function, and
cognition.
The patient will display adequate perfusion as evidenced by stable vital signs and hemodynamics.
Interventions:
 Assess and obtain an accurate patient history.
 Assess and monitor neurological status frequently.
 Assess and monitor vital signs.
 Evaluate diagnostic studies
 Evaluate and monitor pupillary responses
 Monitor the patient’s bilateral motor responses
 Maintain head or neck in midline or neutral position
 Provide rest periods between care activities and limit the duration of procedures.
 Administer IV fluids. (Hypotonic and dextrose-containing fluids should be avoided.)
 Administer supplemental oxygen as needed

59.  Administer medications as indicated (Diuretics such as mannitol may be prescribed
to reduce brain swelling, which helps improve cerebral blood flow and oxygenation.)
 Prepare for surgical intervention as indicated. (Craniotomy may be indicated to help
remove bone fragments, elevate depressed fractures, control hemorrhage, evacuate
hematoma, and debride necrotic tissues, relieving pressure.)

60. 2. Acute Confusion related to (brain injury, neurologic trauma, decreased level of
consciousness) as evidenced by (cognitive dysfunction, misperception, agitation or
restlessness)
Goals:
 The patient will maintain a baseline level of consciousness and will not experience
decreased memory.
 The patient will be able to respond appropriately to questions.
Interventions:
 Assess sensory awareness.
 Assess changes in orientation and personality.
 Assess the patient’s level of cognitive impairment.
 Ensure patient safety.
 Reorient the patient as needed.
 Keep explanations and activities short and simple.
 Eliminate extraneous noise as necessary.
 Provide structured therapies and activities. (This will help promote consistency and
reassurance, reduces the patient’s anxiety and confusion, and promotes a sense of control.)

61. 3. Impaired Physical Mobility
 Assess the patient’s mobility and range of motion regularly.
 Encourage early mobilization and ambulation as tolerated to prevent
complications such as muscle weakness, joint contractures, and deep
vein thrombosis.
 Provide assistive devices, such as walkers or handrails, to support safe
ambulation.
 Collaborate with physical therapy to develop a customized
rehabilitation plan for the patient’s specific needs and limitations.

62. 4. Acute Pain:
 Assess the patient’s pain level using a pain scale and ask about the
location, intensity, and quality of the pain.
 Administer prescribed pain medication, such as analgesics or
nonsteroidal anti-inflammatory drugs (NSAIDs), as ordered to relieve
pain.
 Implement non-pharmacological pain management techniques, such as
positioning, relaxation exercises, or distraction techniques.
 Monitor the patient’s response to pain medication and reassess pain
levels regularly.
 Provide a calm and quiet environment to minimize external stimuli that
may exacerbate pain or discomfort.

63. 5. Risk for seizure
Interventions to prevent trauma or injury during seizures.
 Teach patients and significant others to identify and familiarize warning signs for seizures. Educate on how to
care for patients during and after seizure attacks.
 Monitor and record type, onset, duration, and characteristics of seizure activity.
 Avoid using thermometers that can cause breakage. Use a tympanic thermometer when taking a temperature
reading.
 Uphold strict bedrest if prodromal signs or aura experienced.
 Turn head to side during seizure activity to allow secretions to drain out of the mouth, minimizing the risk of
aspiration and suction airway as indicated.
 Support head, place on a padded area, or assist to the floor if out of bed.
 Put away all possible hazards in the room, such as razors, medications, and matches.
 Do not restrain the patient.
 Monitor and document antiepileptic drug levels, corresponding side effects, and frequency of seizure activity.
 Maintain a lying position on, flat surface. Turn head to side during a seizure to help maintain the tongue from
blocking the airway. Remove any objects near the patient.
 Loosen clothing from neck or chest and abdominal areas; suction as needed.
 Supervise supplemental oxygen or bag ventilation as needed postictally.
 Enforce education about the disease.

64. 6. Risk for Impaired Verbal Communication:
 Assess the patient’s ability to communicate verbally and provide
alternative means of communication, such as using a communication
board or picture cards.
 Use clear and simple language when communicating with the patient,
allowing them ample time to process information and respond.
 Collaborate with speech therapy to assess and manage any speech or
language impairments and provide appropriate interventions.

67. 7. Deficient Knowledge related to (cognitive dysfunction, inadequate access to resources,
inadequate awareness of resources, inadequate knowledge of resources, misinformation,
neurobehavioral manifestations.) as evidenced by (inappropriate behavior, inaccurate
statements about topics related to the condition, inaccurate follow-through of instructions,
development of further complications)
Goals:
 Assess the patient’s cognitive ability.
 Assess the patient’s support system.
 Encourage the patient to participate in developing a relevant treatment regimen.
 Encourage the patient and family to participate in required therapies.
 Discuss possible changes in behavior, mood, and personality at home.
 Discuss the importance of follow-up care.
 Instruct the family to develop a structured and consistent home routine.