HEAD INJURY:-

FUNCTIONAL AREAS OF THE BRAIN:

Frontal Lobe:

 Prefrontal Cortex:– Executive functions (e.g., personality & recognizing consequence)

 Primary Motor Cortex:– Motor Performance (e.g., initiation of voluntary movement as well as the
premotor and supplementary motor areas, which coordinate the planning and initiation of voluntary
movement)
 Broca’s area:– Production of language

– Damage causes Broca’s aphasia, a condition in which the patient understands many
written and spoken words, but has difficulty speaking them

Parietal Lobe:

-Associated with integrating sensory information, contains the spatial orientation system, and is involved in
the comprehension of language

 Primary somatosensory cortex:– Concerned with processing of proprioceptive and tactile stimuli
 Parietal Cortex:– Controls aspects of spatial orientation and directing attention
 Wernicke’s area:– Located partially in the parietal lobe

– Involved in recalling, recognizing, and interpreting words and other sounds in

the process of using language

Occipital Lobe:

 Chiefly responsible for visual functions

 Contains the primary visual cortex and the majority of the visual association area, involved in
higher order processing of visual information

Temporal Lobe:-Contains the primary auditory cortex and part of Wernicke’s area

-Medial parts of the temporal lobe are involved in aspects of memory and learning

INTRODUCTION:-
A head injury is any sort of injury to the brain, skull or scalp. This can range from mild bump or
bruise to a traumatic brain injury. Common head injuries include concussions, skull fractures, and scalp
wounds. The consequences and treatments vary greatly, depending on what caused the brain injury and
how severe it is.
 It can be hard to assess that how severe a head injury is by looking. Some minor head injuries bleed
a lot, while some major injuries don’t bleed at all. It’s important to treat all head injuries seriously and get
them assessed by a doctor.

DEFINITION:-
Head injury includes any trauma to the scalp, skull, or brain also known as traumatic brain injury
(TBI).

INCIDENCE:-
Statistics regarding the occurrence of head injuries are incomplete because many victims die at injury scene
or because the condition is considered minor and health care services are not sought. In India about 1.6
million sustain TBI and seek medical aid, and out of these 10% die. Males are five times more prone to
TBI than females.

CAUSES:-
 RTA (Road Traffic Accidents)
 Assaults
 Sports- related trauma
 Recreational injury
 Firearms
 War-related injuries

PROGNOSIS:-
Head trauma has a high potential for a poor outcome. Deaths from head trauma occur at three points after
injury: immediately after the injury, within 2 hours after injury, and approximately 3 weeks after injury.

Factors that predict a poor outcome includes-

 Intracranial hematoma
 Increased age of patient
 Abnormal motor responses
 Impaired eye movements or papillary light response.
 Early sustained Hypertension
 Increased ICP more than 20 mm-Hg

TYPES OF HEAD INJURY WITH CLINICAL FEATURES:-

Scalp Lacerations:-

- easy to recognize these types of external head trauma

 - Since scalp contains many blood vessels with poor constrictive abilities, scalp
lacerations lead to profuse bleeding. Even small wounds results in significant bleeding.

- Major complication- Bleeding, Infection

Skull fracture:-

It can be described in several ways: (a) linear or depressed (b) simple, comminuted, or
compound and (c) closed or open. Fractures may be closed or open, depending on the presence of a scalp
laceration or extension of the fracture into the air sinuses or dura. The type of severity of a skull fracture
depend on the velocity, momentum, direction and shape of the injuring agent, and site of impact.

Clinical manifestations:- The location of the fracture determines the clinical manifestations. As
examples-

Frontal fractures:
 Exposure of brain to contaminants through frontal air sinus, possible association with air
in forehead tissue
 CSF rhinorrhea
 Pneumocranium (air between cranium and dura mater)

Orbital fracture:

 Periorbital ecchymosis (raccoon eyes)

 Optic nerve injury

Temporal fracture:

 Boggy temporal muscle because of extravasation of blood

 Oval shaped bruise behind ear in mastoid region (Battle”s sign)
 CSF otorrhea
 Middle meningeal artery disruption
 Epidural hematoma

Parietal fracture:

 Deafness
 CSF or brain otorrhea
 Bulging of tympanic membrane caused by blood or CSF
 Facial paralysis
 Loss of taste
 Battle’s sign

Posterior fossa fracture:

 Occipital bruising resulting in cortical blindness

 Visual field defects
  Rare appearance of atarexia or other cerebellar signs

Basilar skull fracture:

 CSF or brain otorrhea

 Bulging or tympanic membrane caused by blood or CSF
 Battle’s sign
 Tinnitus or hearing difficulty
 Rhinorrhea
 Facial paralysis
 Conjugate deviation of gaze
 Vertigo

Types of skull injuries:-

Linear- Break in continuity of bone without alteration of relationship of parts. It causes low velocity
injuries.

Depressed- Inward indentation of skull. It causes powerful blow.

Simple- Linear or depressed skull fracture without fragmentation or communicating lacerations. It causes
Low moderate impacts.

Comminuted- Multipler linear fracture with fragmentationof bonme into many pieces. It causes direct,
high momentum impact.

Compound- Depressed skull fracture and scalp laceration with communicating pathway to intracranial
cavity. It causes severe head injury.

MINOR INJURY:

DIFFUSE INJURY:-

Concussion (a sudden transient mechanical head injury with disruption of neural activity and a
change in the LOC) is considered a minor diffuse head injury. The patient may or may not lose total
consciousness with this injury.

Typical signs of concussion:-

 Brief disruption in LOC

 Amnesia regarding the event (retrograde amnesia)
 Headache
 The manifestations are generally of short duration. If the patient has not lost consciousness, or if the
loss of consciousness lasts less than 5 minutes, the patient is usually discharged from the care facility with
instructions to notify the health care provider if symptoms persist or if behavioral changes are noted.

Postconcussion syndrome may develop in some patients, usually anywhere from 2 weeks to 2
months after the injury. Symptoms include-

 Persistent headache
 Lethargy
 Personality and behavioral changes
 Shortened attention span,
 Decreased short-term memory
 Changes in intellectual ability.

This syndrome can significantly affect the patient's abilities to perform activities of daily living.

Although concussion is generally considered benign and usually resolves spontaneously, the
symptoms may be the beginning of a more serious, progressive problem, especially in a patient with a
history of prior concussion or head injury. At the time of discharge, it is important to give the patient and
the caregiver instructions for observation and accurate reporting of symptoms or changes in neurologic
status.

DIFFUSE AXONAL INJURY:-

Diffuse axonal injury (DAI) is wide spread axonal damage occurring after a mild, moderate, or
severe TBI. The damage occurs primarily around axons in the sub-cortical white matter of the cerebral
hemispheres, basal ganglia, thalamus, and brainstem. Initially, DAI was believed to occur from the tensile
forces of trauma that sheared axons, resulting in axonal disconnection. There is increasing evidence that
axonal damage is not preceded by an immediate tearing of the axon from the traumatic impact, but rather
the trauma changes the function of the axon, resulting in axon swelling and disconnection. This process
takes approximately 12 to 24 hours to develop and may persist longer.

The clinical signs of DAI-

 Decreased LOC, increased ICP

 Decortication or decerebration
 Global cerebral edema.

Approximately 90% of patients with DAI remain in a persistent vegetative state. Patients with DAI
who survive the initial event are rapidly triaged to an ICU, where they will be vigilantly watched for signs
of increased ICP and treated accordingly.
FOCAL INJURY:-

Focal injury can be minor to severe and can be localized to an area of injury. Focal injury consists
of lacerations, contusions, hematomas, and cranial nerve injuries.

Lacerations involve actual tearing of the brain tissue and often occur in association with depressed
and open fractures and penetrating injuries. Tissue damage is severe, and surgical repair of the laceration is
impossible because of the nature of brain tissue. Medical management consists of antibiotics until
meningitis is ruled out, and prevention of secondary injury related to increased ICP. If bleeding is deep into
the brain tissue, focal and generalized signs develop.

When major head trauma occurs, many delayed responses are seen. Such as-

 Hemorrhage, hematoma formation

 Seizures
 Cerebral edema
 Intracerebral hemorrhage is generally associated with cerebral laceration. This hemorrhage
manifests as a space-occupying lesion accompanied by unconsciousness, hemiplegia on the
contralateral side, and a dilated pupil on the ipsilateral side. As the hematoma expands,
signs of increased ICP become more severe. Prognosis is generally poor for the patient with
a large intra-cerebral hemorrhage.

Subarachnoid hemorrhage and intra-ventricular hemorrhage can also occur as secondary to head
trauma.

CONTUSION:-

A contusion is bruising of the brain tissue within a focal area. It is usually associated with a closed
head injury. A contusion may contain areas of hemorrhage, infarction, necrosis, and edema, and it
frequently occurs at a fracture site.

With contusion, the phenomenon of coup-contrecoup injury is often noted, and injuries can range
from minor to severe. Damage from coup-contrecoup injury occurs when impact injury mechanisms.

Contusions or lacerations occur both at the site of the direct impact of the brain on the skull (coup)
and at a secondary area of damage on the opposite side away from injury (contrecoup), leading to multiple
contused areas. Contrecoup injuries tend to be more severe, and overall patient prognosis depends on the
amount of bleeding around the contusion site.

Contusions may continue to bleed or re-bleed and appear to "blossom" on subsequent CT scans of
the brain, which worsens the neurologic outcome. Neurologic assessment may demonstrate focal and
generalized manifestation, depending on the contusion's size and location. Seizures are a common
complication of brain contusion, especially in the first 7 days after injury. Anticoagulant use and
coagulopathy are associated with increased hemorrhage, more severe head injury, and a higher mortality
rate. This is especially important when considering older individuals who are taking warfarin or aspirin at
home. If they fall, their contusion is likely to be more severe due to the use of anticoagulants. Thus risk for
falls should be assessed.

COMPLICATIONS:-
Epidural Hematoma-

An epidural hematoma results from bleeding between the dura and the inner surface of the skull. An
epidural hematoma is a neurologic emergency and is usually associated with a linear fracture crossing a
major artery in the dura, causing a tear. It can have a venous or an arterial origin. Venous epidural
hematomas are associated with a tear of the dural venous sinus and develop slowly. With arterial
hematomas, the middle meningeal artery lying under the temporal bone is often torn. Hemorrhage occurs
into the epidural space, which lies between the dura and inner surface of the skull. Because this is an
arterial hemorrhage, the hematoma develops rapidly.

Signs Of An Epidural Hematoma:-

 Initial period of unconsciousness at the scene, with a brief lucid interval followed by a decrease in
LOC.
 Headache, nausea and vomiting
 Focal findings.

Rapid surgical intervention to evacuate the hematoma and prevent cerebral herniation, along with
medical management for increasing ICP, can dramatically improve outcomes.

Subdural Hematoma:-

A subdural hematoma occurs from bleeding between the dura mater and the arachnoid layer of the
meninges. A subdural hematoma usually results from injury to the brain tissue and its blood vessels. The
veins that drain from the surface of the brain into the sagittal sinus are the source of most subdural
hematomas. Because it is usually venous in origin, the subdural hematoma may be slower to develop.
However, a subdural hematoma may be caused by an arterial hemorrhage, in which case it develops more
rapidly.

Subdural hematomas may be acute, subacute, or chronic.

The signs and symptoms:-

An acute subdural hematoma manifests within 24 to 48 hours of the injury. Sign and symptoms are-

 Decreasing LOC and headache.

 The size of the hematoma determines the patient's clinical presentation and prognosis. The patient's
appearance may range from drowsy and confused to unconscious.
 The ipsilateral pupil dilates and becomes fixed if ICP is significantly elevated. Blunt force injuries
that produce acute subdural hematomas may also cause significant underlying brain injury,
 resulting in cerebral edema. The resulting increase in ICP from the cerebral edema can cause an
increased morbidity and mortality risk.

A subacute subdural hematoma usually occurs within 2 to 14 days of the injury. Signs and symptoms are-

 Initial bleeding
 A subdural hematoma may appear to enlarge over time as the breakdown products of the blood
draw fluid into the subdural space.

A chronic subdural hematoma:-

It develops over weeks or months after a seemingly minor head injury. Chronic subdural hemato
mas are more common in older adults because of a potentially larger subdural space.

Sign and symptoms-

 Brain atrophy- With atrophy, the brain remains attached to the supportive structures
 Increased tension
 Tearing.
 Because the sub dural space is larger, the presenting complaint is focal symptoms

Intracerebral Hematoma:-

Intracerebral hematoma occurs from bleeding within the brain tissue in approximately 16% of head
injuries. It usually occurs within the frontal and temporal lobes, possibly from rupture of intracerebral
vessels at the time of injury. The size and location of the hematoma are key determinants of the patient's
outcome.

DIAGNOSTIC EVALUATION:-
1. CT scan is the best diagnostic test to evaluate for head trauma because it allows rapid diagnosis and
intervention in the acute care setting.
2. MRI, PET
3. evoked potential studies may also be used in the diagnosis and differentiation of head injuries. An
MRI scan is more sensitive than the CT scan in detecting small lesions.
4. Transcranial Doppler studies allow for the measurement of CBF velocity.
5. A cervical spine x-ray series, CT scan, or MRI of the spine may also be indicated, since cervical
spine trauma often occurs at the same time as a head injury. In general, the diagnostic studies are
similar to those used for a patient with increased ICP.

The principal treatment of head injuries is timely diagnosis and surgery (if necessary). For the patient
with concussion and contusion, observation and management of increased ICP are the primary
management strategies.
TREATMENT-
 The treatment of skull fractures is usually conservative.
 For depressed fractures and fractures with loose fragments, a craniotomy is necessary to elevate the
depressed bone and remove the free fragments.
 If large amounts of bone are destroyed, the bone may be removed that is known as craniectomy,
and a cranioplasty will be needed later.
 In cases of large acute subdural and epidural hematomas, or those associated with significant
neurologic impairment, the blood must be removed through surgical evacuation. A craniotomy is
generally performed to visualize and allow control of the bleeding vessels.
 Burr-hole openings may be used in an extreme emergency for a more rapid decompression,
followed by a craniotomy. A drain may be placed postoperatively for several days to prevent re-
accumulation of blood. In cases where extreme swelling is expected (e.g., DAI, hemorrhage), a
craniectomy may be performed, which involves removing a piece of skull to reduce the pressure
inside the cranial vault, thus reducing the risk of herniation.

NURSING ASSESSMENT:-
1. Obtained objective data by applying the GCS assessing and monitoring the neurologic status,
2. Determine whether a CSF leak has occurred.
3. Ensure patent airway
4. Stabilize cervical spine.
5. Administer 0₂ via non-rebreather mask.
6. Establish IV access with two large-bore catheters to infuse normal saline or lactated Ringer's
solution.
7. Intubate if GCS score <8.
8. Control external bleeding with sterile pressure dressing.
9. Remove patient's clothing.
10. Ongoing Monitoring
11. Maintain patient warmth using blankets, warm IV fluids, overhead warming lights, warm
humidified 0₂.
12. Monitor vital signs, level of consciousness, O₂ saturation, cardiac rhythm, GCS score, pupil size
and reactivity.
13. Anticipate need for intubation if gag reflex is impaired or absent.
14. Assume neck injury with head injury.
15. Assess for rhinorrhea, otorrhea, scalp wounds.
16. Administer fluids cautiously to prevent fluid overload and increasing ICP.

INURSING DIAGNOSES:-

1. Risk for ineffective cerebral tissue perfusion related to interruption of CBF associated with cerebral
hemorrhage, hematoma, and edema.
2. Hyperthermia related to increased metabolism, infection, and hypothalamic injury.
 3. Impaired physical mobility related to decreased LOC
4. Anxiety related to abrupt change in health status, hospital environment, and uncertain future
5. Potential complication: increased ICP related to cerebral edema and hemorrhage

PLANNING:-

The overall goals are that the patient with an acute head injury will-

(1) maintain adequate cerebral oxygenation and perfusion;

(2) remain normothermic;

(3) achieve control of pain and discomfort;

(4) be free from infection;

(5) have adequate nutrition;

(6) attain maximal cognitive, motor, and sensory function.

NURSING IMPLEMENTATION:-

HEALTH PROMOTION-

1. Prevent car and motorcycle collisions. The use of helmets by cyclists has led to fewer TBIs.
2. Advice everyone about the use of car seat belts and child car seats is also associated with reduced
TBI mortality rates.
3. Be active in campaigns that promote driving safety
4. Speak to driver education classes regarding the dangers of unsafe driving and of driving after
drinking alcohol and using drugs. Wearing seat belts in cars and helmets for riding on motorcycles
is the most effective measure for increasing survival after crashes.
5. Protective helmets should also be worn by lumberjacks, construction workers, miners, horseback
riders, bicycle riders, snowboarders, and skydivers.
6. Individuals who are at risk for falls (e.g., older adults) should be evaluated for safety in the home,
since falls are the second leading cause of head injuries.

ACUTE INTERVENTION:-

1. Management at the injury scene can have a significant impact on the outcome of the head injury.
The general goal of nursing management of the head-injured patient is to maintain cerebral
oxygenation and perfusion and prevent secondary cerebral ischemia.
2. Surveillance or monitoring for changes in neurologic status is critically important because the
patient's condition may deteriorate rapidly, necessitating emergency surgery. Appropriate
preoperative and postoperative nursing interventions are initiated if surgery is anticipated.
 3. Explain the need for frequent neurologic assessments to both the patient and the caregiver.
Behavioral manifestations associated with head injury can result in a frightened, disoriented patient
who is combative and resists help. A family member may be available to stay with the patient and
thus decrease anxiety and fear. One of the most important needs for the caregiver and family
members in the acute injury phase is information about the patient's diagnosis, treatment plan, and
rationale for the interventions.
4. Perform neurologic assessments at intervals based on the patient's condition. The GCS is useful in
assessing the LOC. Indications of a deteriorating neurologic state, no matter how subtle, such as a
decreasing LOC or decreasing motor strength, should be reported to the health care provider.
Monitor the patient's condition closely.
5. The major focus of nursing care for the brain-injured patient relates to increased ICP. However,
some problems may require specific nursing intervention.
6. Eye problems may include loss of the corneal reflex, periorbital ecchymosis and edema, and
diplopia. Loss of the corneal reflex may necessitate administering lubricating eyedrops or taping the
eyes shut to prevent abrasion. Periorbital ecchymosis and edema decrease with time, but cold and,
later, warm com presses provide comfort and hasten the process. Diplopia can be relieved by use of
an eye patch. Consider a consult with an ophthalmologist.
7. Hyperthermia may occur from injury to or inflammation of the hypothalamus. Elevations in body
temperature can result in increased CBF, cerebral blood volume, and Increased ICP.

AMBULATORY AND HOME CARE:-

Once the condition has stabilized, the patient is usually transferred for acute rehabilitation
management. There may be chronic problems related to motor and sensory deficits, communication,
memory, and intellectual functioning. Many of the principles of nursing management of the patient with a
stroke are appropriate for these patients.

Conditions that may require nursing and collaborative management include-

 Poor nutritional status

 bowel and bladder management,
 spasticity,
 dysphagia,
 deep vein thrombosis,
 and hydrocephalus.

The patient's outward appearance is not a good indicator of how well he or she will ultimately
function in the home or work environment. The outward physical appearance does not necessarily reflect
what has happened in the brain.

In all cases, the family must be given special consideration. They need to understand what is
happening and be taught appropriate interaction patterns. Prepare the family for the patient's emergence
from coma and explain that the process of awakening often takes several weeks.
 When it is the time for discharge planning, the patient, care giver, and family may benefit from
specific posthospitalization instructions to avoid family-

 Patient friction.
 Special "no" policies that may be appropriately suggested by the neurosurgeon, neuropsychologist,
and nurse include no drinking of alcoholic beverages, no driving, no use of firearms, no working
with hazardous implements and machinery, and no unsupervised smoking.
 Family members, particularly spouses, go through role transition as the role changes from that of
spouse to that of caregiver.

EVALUATION:-
The expected outcomes are that the patient with a head injury will-

 Maintain normal CPP

 Achieve maximal cognitive, motor, and sensory function.
 Experience no infection or hyperthermia

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