Introduction

Head injury is the most common cause of death from trauma in the united states.
Approximately 1 million people receive treatment for head injuries every year. Traumatic brain
injury is the most serious form of head injury.the most common causes of traumatic brain injury
are motor vehicle crashes, violence, and falls. Groups at highest risk for traumatic brain injury
are persons age 15 to 24 years and males, who suffer traumatic brain injury at a rate almost twice
that of females.the very young (under 5) and the very old (over 75) are also atincreased risk. It is
estimated that 5.3 million americans today are living with a disability as a result of a traumatic
brain injury. The best approach to head injury is prevention

DEFINITION

Head injury is injury involving scalp, skull and brain

INCIDENCE

Groups at highest risk for traumatic brain injury are persons age 15 to 24 years and
males, who suffer traumatic brain injury at a rate almost twice that of females. The very young
(under 5) and the very old (over 75) are also at increased risk. It is estimated that 5.3 million
americans today are living with a disability as a result of a traumatic brain injury

ETIOLOGY

 Motor vehicle accident

 Falls
 Assaults
 Gun shot wound

CLASSIFICATION OF HEAD INJURY

1.glasgow coma score

Severity of head injury is classified according to the glasgowcoma score (gcs) in particular the
motor score – is the best predictor of neurological outcome:

• minor head injury: gcs 15 with no loss of consciousness (loc);

• mild head injury: gcs 14 or 15 with loc;

• moderate head injury: gcs 9–13;

• severe head injury: gcs 3–8.

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2.blunt vs. PenetratingHead injury may be classified as blunt or penetrating. Penetratinghead
injuries are f urther divided into low-velocity injuries such as those caused by stabbing and high-
velocity injuries such as gunshot injuries .

3.morphological

A head injury may be classified according to the type of injury that has occurred

 Scalp injury
 Skull fractures
 Brain injury

CLASSIFICATION OF HEAD INJURY

Abrasion (brushwound),

Contusion,

SCALPINJURY Laceration,

Hematoma (subgleal hematoma)

Large avulsions of the scalp

on the basis of pattern

1.linear

HEAD INJURY 2.depressed

3.simple
4.comminuted
SKULL FRACTURES 5.compound

on the basis of area involved

Frontal fracture

Orbital fracture
Temporal fracture
Parietal fracture

Posterior fossa fracture

Basilar skull fracture
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 1.Closed (blunt) brain

2.open brain injury

BRAIN INJURY Major injury

Contution

Diffuse axonal injury

Intracranial hemorrhage

Epidural hematoma

Subdural hematoma
Intracerebral hemorrhage

Minor - concussion

PATHOPHYSIOLOGY

Primary injury and secondary injury.

Primary injury

Is the initial damage to the brain that results from the traumatic event.this may include
contusions, lacerations, and torn blood vessels from impact, acceleration or foreign object
penetration

Secondary injury

Occur hours and day after the initial injury and is due primarily to brain swelling
or ongoing bleeding.An injured brain is different from other injured body areas due to its unique
characteristics. It resides within the skull, which is a rigid closed compartment . Unlike an
injured ankle, in which the covering skin expands with swelling, the confines of the skull do not
allow for the expansion of cranial contents. Thus, any bleeding or swelling within the skull
increases the ICP

Volume of contents within a container of fixed size and so can cause increased
intracranial pressure. If the increased pressure is high enough, it can cause a downward or lateral
displacement of the brain through or against the rigid structures of the skull. This causes
restriction of blood flow to the brain, decreasing oxygen delivery and waste removal. Cells

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within the brain become anoxic and cannot metabolize properly, producing ischemia, infarction,
irreversible brain damage, and eventually brain death.

Brain suffers traumatic injury

Brain swelling or bleeding

Intracranial volume

Rigid cranium allows no room for expansion

Of contents ,so intracranial pressure increases

Pressure on blood vessels within the brain

Causes blood flow to the brain to slow

Cerebral hypoxia and ischemia occur

Intracranial pressure continues

To rise. Brain may herniate

Cerebral blood flow ceases

SIGNS AND SYMPTOMS

integumentary
lacerations, contusions, abrasions, hematoma, battle's sign, periorbital edema (raccoon eyes)and
ecchymosis, otorrhea, exposed brain matter
respiratory
rhinorrhea, impaired gag reflex, inability to maintain a patent airway ,impending hemiation:
altered/irregular respiratory rate and pattern
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cardiovascular
impending herniation: cushing's response (systolic hypertension [wider pulse pressure)],
bradycardia [full and bounding pulse])
gastrointestinal
vomiting, projectile vomiting, bowel incontinence
urinary
bladder incontinence
reproductive
uninhibited sexual expression
neurologic
altered level of consciousness, seizure activity, pupil dysfunction, cranial deficit,anisochoria
musculoskeletal
Decorticate or decerebrate posturing /muscular rigidity /increased tone flaccidity, ataxia

Other symptoms

Pain :persistent, localized pain usually suggests that a fracture is present. Fractures of the cranial
vault may or may not produce swelling in the region Of the fracture

Hemorrhage :from the nose, pharynx, or ears, and blood may appear Under the conjunctiva. An
area of ecchymosis (bruising) may be seen over the mastoid (battle’s sign).

CSF leakage

Basal skull fractures are suspected when cerebrospinal fluid escapes from the ears (csf otorrhea)
and the nose (csf rhinorrhea). A halo sign (a blood stain surrounded by a yellowish stain) may be
seen on bed linens or the head dressing and is highly suggestive of a csf leak.

Bloody CSF

Suggests a brain laceration or contusion.

Occular changes

Anisocoria or an asymmetrical sluggish response may suggest partial third nerve dysfunction
occipital bruising resulting in cortical blindness, visual field defects, periorbital ecchymosis
(raccoons eyes}

Altered neurological status

It can extent from confusion to coma ,behaviral changes,amnesia[amnesia may be antegrade (for
events after the injury) or retrograde (for events preceding the injury}

ASSESSMENT AND DIAGNOSTIC FINDINGS

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History

 Cause of injury/mechanism of injury

 Surgical history
 Loss of consciousness or amnesia
 Level of consciousness at scene and on transfer
 Evidence of seizures
 Probable hypoxia or hypotension
 Pre-existing medical conditions
 Medications (especially anticoagulants)
 Illicit drugs and alcohol
 Physical examination

Physical Examination

■ glasgow coma score

■ pupil size and response

■ signs of base of skull fracture

1. Bilateral periorbital oedaema (raccoon eyes)

2. Battle’s sign (bruising over mastoid)
3. Cerebrospinal fluid rhinorrhoea or otorrhoea
4. Haemotympanum or bleeding from ear

■ full neurological examination: tone, power, sensation and Reflexes

Computed tomography (CT) scan

X-rays

Magnetic resonance imaging (MRI)

Cerebral angiography

SCALP INJURY

Isolated scalp trauma is generally classified as a minor head injury.the scalp bleeds profusely
when injured

Types of scalp injury

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  Abrasion (brushwound),
 Contusion,
 Laceration,
 Hematoma beneath the layers of tissue of the scalp (subgleal hematoma)
 Large avulsions of the scalp

Diagnosis of any scalp injury is based on physical examination ,inspection, and

palpation.

Management

Scalp wounds are potential portal of entry of organisms that cause intracranial infections.
There fore,the area is irrigated before the laceration is sutured to remove foreign material and to
reduce the risk for infection. Subgleal hematomas (hematomas below the outer covering of the
skull) usually absorb on their own and do not require any specific treatment.

1.primary suturing in simple lacerations ,sharp, without tissue loss and gross contamination

2.secondary intention in wounds with minimum tissue loss

3.debridement and a split thickness graft in wounds with extensive tissue loss and intact
pericranium

4.local flaps in wounds with extensive tissue loss and stripped Pericranium and a split thickness
graft for donor area (if a defect is left)

5Pedicular flaps can be used if local flaps are not sufficient especially for occipital areas and
small defects

6.Free tissue transplant is used for anterior and large areas

SKULL FRACTURES

A skull fracture is a break in the continuity of the skull caused by forceful trauma. It may occur
with or without damage to the brain.

Type of skull fracture on the basis of pattern

1.linear
break in continuity of bone without alteration of relationship of parts

2.depressed
inward indentation of skull
3.simple
linear or depressed skull fracture without fragmentation or communicating lacerations

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4.comminuted
multiple linear fractures with fragmentation of bone to many pieces
5.compound
depressed skull fracture and scalp laceration with communicating pathway to intracranial
cavity

Type of skull fracture on the basis of area involved

Frontal fracture

Exposure of brain to contaminants through frontal sinus, possible association with air in forehead
tissue rhinorrhea, or pneumocranium

Orbital fracture

Periorbital ecchymosis (raccoons eyes}

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 fracture

Deafness, csf or brain otorrhea, bulging of tympanic membrane caused by blood or csf, battle's-
sign, tinnitus
Posterior fossa fracture

Occipital bruising resulting in cortical blindness, visual field defects, rare appearance of ataxia
or other signs

Basilar skull fracture

CSF or brain otorrhea, bulging of tympanic membrane caused by blood or csf, battle's-sign,
tinnitus or hearing difficulty, rhinorrhea, facial paralysis,conjugate deviation of gaze, vertigo

MANAGEMENT

Nondepressed skull fractures

Generally do not require surgical treatment; however, close observation of the patient is
essential. Nursing personnel may observe the patient in the hospital, but if no underlying brain
injury is present, the patient may be allowed to return home. If the patient is discharged home,
specific instructions must be given tothe family.

Depressed skull fractures

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 Managed conservatively,only contaminated or deforming fractures require surgery.if
surgery is necessary, the scalp is shaved and cleansed with copious amounts of saline to remove
debris. The fracture is then exposed. After the skull fragments are elevated, the area is
débrided.large defects can be repaired immediately with bone or artificial grafts; if significant
cerebral edema is present, repair of the defect can be delayed for 3 to 6 months

 Comminuted(replacement as a Cranioplasty if not infected with treatment of other

associated injuries)

 Linear fractures (no treatment but observation if closed, debridement if infected and
compound)
 Depressed(replacement as a cranioplastyif not infected, otherwise good debridement and
craniectomy)
 Basilar skull fracture (observation for two days, avoid irrigation of the nose or ear,
avoid probing, detailed auditory and vestibular examination is performed at6 weeks
interval)

 Frontal sinus fracture (if in the posterior wall cranializationis necessary)

BRAIN INJURY

The most important consideration in any head injury is whether minor injury can cause
significant brain damage secondary to obstructed blood flow and decreased tissue perfusion. The
brain cannot store oxygen and glucose to any significant degree. Because the cerebral cells need
an uninterrupted blood supply to obtain these nutrients, irreversible brain damage and cell death
occur when the blood supply is interrupted for even a few minutes

1.Closed (blunt) brain and open brain injury

a).closed (blunt) brain Injury occurs when the head accelerates and then rapidly decelerates or
collides with another object and brain tissue is damaged, but there is no opening through the
skull and dura.

b)Open brain injury occurs when an object penetrates the skull, enters the brain, and damages
the soft brain tissue in its path (penetrating injury), or when blunt trauma to the head is so severe
that it opens the scalp, skull, and dura toexpose the brain.

Brain injuries is again classified into minor head injury and major head injury.

2.Minor head injury include

a)Concussion

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 A cerebral concussion after head injury is a temporary loss of neurologic
function with no apparent structural damage. A concussion generally involves a period of
unconsciousness lasting from a few seconds to a few minutes. The jarring of the brain may be so
slight as to cause only dizziness and spots before the eyes(“seeing stars”), or it may be severe
enough to cause complete lossof consciousness for a time. If the brain tissue in the frontal lobe
is affected, the patient may exhibit bizarre irrational behavior,whereas involvement of the
temporal lobe can produce temporaryamnesia or disorientation.

. Treatment involves observing the patient for headache,dizziness, lethargy,

irritability, and anxiety. The occurrence of these symptoms after injury is referred to as post
concussion syndrome.family is instructed to observe for the following signs and symptoms and
to notify the physician or clinic (or bring the patient to the emergency department) if they occur:

• difficulty in awakening

• difficulty in speaking

• confusion

• severe headache

• vomiting

• weakness of one side of the body

MAJOR HEAD INJURY

b)Contusion

Cerebral contusion is a more severe injury in which the brain is bruised, with
possible surface hemorrhage. The patient is unconscious for more than a few seconds or minute.
Patient prognosis is dependent upon the amount of bleeding around the contusion site, which can
range from minimal to severe.
Contusions may continue to bleed or re bleed which worsens neurologic
outcome. Anticoagulant use and coagulopathy are associated with increased hemorrhage and
head injury. Seizures are a common complication of brain contusion.lacerations involve actual
tearing occur in association with depressed and open fractures and penitrating injuries.

c)Diffuse axonal injury

Diffuse axonal injury involves widespread damage to axons in the cerebral hemispheres, corpus
callosum, and brain stem. It can be seen in mild, moderate, or severe head trauma and results in
axonal swelling and disconnection. Clinically, with severe injury, the patient may have

1.immediate coma,

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2.decorticate and decerebrate posturing

3.global cerebral edema.

Diagnosis is made by clinical signs in conjunction with a ct scan or mri. Recovery

depends on the severity of the axonal injury.

d)Intracranial hemorrhage

Hematomas (collections of blood) that develop within the cranial vault are the
most serious brain injuries . A hematoma may be

 epidural
 subdural
 intracerebral

A rapidly developing hematoma, even if small, may be fatal,where as a larger but slowly
developing collection of blood may allow compensation for increases in ICP.

1)Epidural hematoma (extradural hematoma Or hemorrhage)

After a head injury, blood may collect in the epidural space between the
skull and the dura. This can result from a skull fracture that causes a rupture or laceration of the
middle meningeal artery, the artery that runs between the dura and the skull inferior to a thin
portion of temporal bone. Hemorrhage from this artery causes rapid pressure on the brain.
Symptoms are caused by the expanding hematoma. Usually, there is a momentary loss of
consciousness at the time of injury, followed by an interval of apparent recovery (lucid interval).
During the lucid interval, compensation for the expanding hematoma takes place by rapid
absorption of csf and decreased intravascular volume, both of which help to maintain a normal
icp. When these mechanisms can no longer compensate, even a small increase in the volume of
the blood clot produces a marked elevation in ICP.then, often suddenly, signs of compression
appear and the patient deteriorates rapidly.

. Treatment

 Consists of making openings through the skull (burr holes) to decrease icp emergently,
remove the clot, and control the bleeding.
 A craniotomy may be required to remove the clot and control the bleeding.
 A drain is usually inserted after creation of burr holes or a craniotomy to prevent
reaccumulation of blood.

2)Subdural hematoma
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 A subdural hematoma is a collection of blood between the dura and the brain, a space
normally occupied by a thin cushion of fluid. The most common cause of subdural hematoma is
trauma,but it may also occur from coagulopathies or rupture of an aneurysm. A subdural
hemorrhage is more frequently venous in origin and is due to the rupture of small vessels that
bridge the subdural space. A subdural hematoma may be

1.Acute

2. Subacute

3.Chronic

Depending on the size of the involved vessel and the amount of bleeding present..

1. Acute and subacute hematomas

These are associated with major head injury involving contusion or

laceration. Clinical symptoms develop over 24 to 48 hours.signs and symptoms include changes
in the level of consciousness(LOC), pupillary signs, and hemiparesis. There may be minor or
even no symptoms with small collections of blood. Coma, increasing blood pressure, decreasing
heart rate, and slowing respiratory rate are all signs of a rapidly expanding mass requiring
immediate intervention.

. If the patient can be transported rapidly to the hospital, an Immediate

craniotomy is performed to open the dura, allowing the subdural clot to be evacuated. Successful
outcome also depends on the control of ICP and careful monitoring of respiratory function

2.Chronic subdural hematoma. Chronic subdural hematomas can develop from seemingly
minor head injuries and are seen most frequently in the elderly. The elderly are prone to this type
of head injury secondary to brain atrophy, which is an expected consequence of the aging
process

.A chronic subdural hematoma resembles other conditions and may be mistaken for a stroke. The
bleeding is less profuse and there is compression of the intracranial contents. The blood within
the brain changes in character in 2 to 4 days, becoming Thicker and darker. In a few weeks, the
clot breaks down and has the color and consistency of motor oil. Eventually, calcification or
ossification of the clot takes place. The brain adapts to this foreign body invasion, and the
clinical signs and symptoms fluctuate. There may be severe headache, which tends to come and
go,Alternating focal neurologic signs; personality changes; mental deterioration;And focal
seizures.

. The treatment of a chronic subdural hematoma consists of surgical evacuation of the clot.
The procedure may be carried out through multiple burr holes, or a craniotomy may be
performed for a sizable subdural mass that cannot be suctioned or drained through burr holes.

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3)Intracerebral hemorrhage and hematoma

Intracerebral hemorrhage is bleeding into the brain. It is commonly seen in head injuries
when force is exerted to the head over a small area .These hemorrhages within the brain may also
result from

 Systemic hypertension, which causes degeneration and rupture of a vessel;

 Rupture of a saccular aneurysm; vascular anomalies;
 Intracranial tumors;
 Systemic causes, including bleeding
 Disorders such as leukemia, hemophilia, aplastic anemia, and Thrombocytopenia
 Complications of anticoagulant therapy.

The onset may be insidious, beginning with the development of neurologic deficits followed by
headache.

MANAGEMENT

 Supportive care
 Control of ICP
 Careful administration of fluids, electrolytes
 Antihypertensive medications.

Surgical intervention

Craniotomy or craniectomy

Permits removal of the blood clot and control of hemorrhage but sometime it may not be possible
because of the inaccessible location of the bleeding or the lack of a clearly circumscribed area of
blood that can be removed.

COMPLICATIONS

Decreased cerebral perfusion

Any decrease in this pressure can impair cerebral perfusion and cause brain hypoxia and
ischemia, leading to permanent damage.

Cerebral edema and herniation

Cerebral edema is the most common cause of increased icp in the patient with a head injury, with
the swelling peaking approximately 48 to 72 hours after injury. Bleeding also may increase the
volume of contents within the rigid closed compartment of the skull,causing increased icp and
herniation of the brain stem and resulting in irreversible brain anoxia and brain death

Impaired fluid, electrolyte, and nutritional balance

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Fluid, electrolyte, and nutritional imbalances are common in the patient with a head injury.
Common imbalances may include hyponatremia, which is often associated with the syndrome of
inappropriate secretion of antidiuretic hormone

Undernutrition is also a common problem in response to the increased metabolic needs

associated with severe head injury. \

Post-traumatic seizures

Patients with head injury are at an increased risk for posttraumatic seizures. Post-traumatic
seizures are classified as immediate (within 24 hours of injury), early (within 1 to 7 days of
injury), or late

MANAGEMENT

Management of mild head injury(GCS 14–15)

1.simple measures to reduce icp include positioning the patient with the head up 20–30
degee[fowlers position (headup) when the spine has not been cleared] and making sure that the
cervical immobilisation collar is not so tight as to restrict Venous return from the head.

2.in patients with pupillary dilatation suggesting acutely raised icp, the administration of 0.5 mg
kg–1 of 20% mannitol will temporarily reduce icp during interhospital transfer or on the way to
theatre. Excessive use of this osmotic diuretic can lead to hypovolaemia and hypotension.

Intracranial pressure monitoring

Icp monitoring is a useful adjunct in the management of unconscious patients with head
injury. A sustained icp of > 20 mmhg is associated with a worse outcome. The icp can also be
used to calculate the cerebral perfusion pressure . An icp monitor may be parenchymal or
ventricular.

Decompressive craniectomy

The purpose of a decompressive craniectomy is to control the ICP in patients without a

focal intracerebral haematoma. The operation involves removing a large section of skull and
opening the dura, allowing the swollen brain to expand underneath the scalp the bone flap is
stored and can be replaced 3–6 months later when the patient has made a good neurological
recovery and the brain swelling has resolved.

MEDICAL MANAGEMENT OF SEVERE HEAD INJURY

.Airway and ventilation

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 A definitive airway is required in cases of severe head injury for several reasons: the
patient in traumatic coma is unable to protect their airway and is at risk of aspiration; gas
exchange may be impaired; the safe interhospital transfer of a patient with an impaired conscious
level and who is at risk of further neurological Deterioration requires intubation and ventilatory
support

Normal gas exchange in the head-injured patient must be confirmed and

maintained. Hypoxia and hypercapnia will result in increased brain ischaemia and secondary
brain injury

Circulation and cerebral perfusion pressure

A single episode of hypotension with a systolic blood pressure of < 90 mmhg is

associated with a worse outcome in traumatic coma. Cerebral perfusion pressure should be
maintained at > 65 mmhg in severely head-injured patients.

Control of intracranial pressure

Normal icp is 8–12 mmhg. A sustained icp of > 20 mmhg is associated with poor
outcome. As

Well as the environmental, respiratory and circulation measures outlined above, measures to

Reduce ICP include:

 Sedation, with or without muscle relaxants.

 Use of diuretics. Judicious use of diuretics such as furosemide and mannitol will
temporarily reduce cerebral swelling and icp.
 Thermoregulation. Pyrexia will increase the brain metabolic rate and should be avoided.
Active cooling to reduce the Metabolic rate
 Use of barbiturates. The use of agents such as thiopentone reduces the brain metabolic
rate and helps reduce icp.barbiturates are associated with respiratory and metabolic
complications and can take days to clear from the body.
 Maintaining fluid and electrolyte balance. Severely brain-injured patients are susceptible
to disturbances of sodium haemostasis such as diabetes insipidus and syndrome of
inappropriate antidiuretic hormone (siadh).
 Seizure control. Seizures increase the brain metabolic rate and should be controlled.
Prophylactic anticonvulsants may reduce seizures in the first week

SURGICAL MANAGEMENT OF RAISED INTRACRANIAL PRESSURE

■ early evacuation of focal haematomas bu burrhole

■ cerebrospinal fluid drainage via ventriculostomy

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■ delayed evacuation of swelling contusions

■ decompressive craniectomy

NURSING MANAGEMENT

Assessment of neurologic signs

• assessment for signs and symptoms of icp elevation

• calculation of cerebral perfusion pressure if icp monitor is in place

• monitoring of antiseizure medication blood levels

Integumentary system

• assessment of skin integrity and character of the skin

• assessment of oral mucous membrane

Musculoskeletal system

• assessment of range of motion of joints and development of

Deformities or spasticity

Gastrointestinal system

Assessment of abdomen for bowel sounds and distention

Genitourinary system

• monitoring for decreased hemoglobin

• intake and output record

Metabolics

Assessment of fluid and electrolyte balance

• recording of weight, if possible

• hematocrit

• electrolyte

Respiratory system

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• assessment of respiratory function

—auscultate chest for breath sounds.

—note the respiratory pattern if possible (not possible if a ventilator is being used).

—note the respiratory rate

—note whether the cough reflex is intact.

• arterial blood gas levels

• complete blood count

• chest x-ray studies

• sputum cultures

• o2 saturation using pulse oximetry

Cardiovascular

• assessment of vital signs

• monitoring for cardiac dysrhythmias

• assessment for deep vein thromboses of legs

• electrocardiogram

• electrolyte studies

• blood coagulation studies

• i125 fibrinogen scan of legs

• blood glucose level

• blood acetone level

• blood osmolality

• urine specific gravity

Psychological/emotional response

• collection of information about the family and the role of the head-injured person within the
family

• assessment of the family to determine how functional it was before the injury occur
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NURSING DIAGNOSIS

Based on the assessment data, the patient’s major nursing diagnoses may include the following:

• ineffective airway clearance and impaired gas exchange related to brain injury

• ineffective cerebral tissue perfusion related to increased icp and decreased cpp

• deficient fluid volume related to decreased loc and hormonal dysfunction

• imbalanced nutrition, less than body requirements, related to metabolic changes, fluid
restriction, and inadequateintake

• risk for injury (self-directed and directed at others) related to seizures, disorientation,
restlessness, or brain damage

• risk for imbalanced (increased) body temperature related to damaged temperature-regulating

mechanism

• potential for impaired skin integrity related to bed rest, hemiparesis, hemiplegia, and
immobility

• disturbed thought processes (deficits in intellectual function, communication, memory,

information processing) related

To brain injury

• potential for disturbed sleep pattern related to brain injury and frequent neurologic checks

• potential for compromised family coping related to unresponsiveness of patient,

unpredictability of outcome, prolonged recovery period, and the patient’s residual physical and
emotional deficit

• deficient knowledge about recovery and the rehabilitation process

NURSING INTERVENTIONS

Vital signs

Vital signs are monitored at frequent intervals to assess the intracranial status

Signs of increasing icp include

Slowing of the heart rate(bradycardia),

Increasing systolic blood pressure

Widening pulse pressure.

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 A rapid rise in body temperature is regarded as unfavorable because hyperthermia
increases the metabolic demands of the brain and may indicate brain stem damage. The
temperature is maintained at less than 38c (100.4f)..

Motor function

 Motor function is assessed frequently by observing spontaneous Movements

 The presence or absence of spontaneous movement of each extremity is also
 Noted, and speech and eye signs are assessed.
 If the patient does not demonstrate spontaneous movement,responses to painful stimuli
are assessed. Motor response to pain is assessed by applying a central stimulus, such as
pinching the

Adequate exchange of air

• keep the unconscious patient in a position that facilitates drainage of oral secretions, with the
head of the bed elevated about 30 degrees to decrease intracranial venous pressure

• establish effective suctioning procedures (pulmonary secretions produce coughing and

straining, which increase icp).

• guard against aspiration and respiratory insufficiency.

• closely monitor arterial blood gas values to assess the adequacy Of ventilation.

• monitor the patient who is receiving mechanical ventilation.

• monitor for pulmonary complications such as acute respiratory distress syndrome and
pneumonia

Monitoring fluid and electrolyte balance

The monitoring of serum electrolyte levels is important, especially in patients receiving

osmotic diuretics, those with inappropriate hormone secretion, and those with post-traumatic
diabetes insipidus.

 .Endocrine function is evaluated by monitoring serum electrolytes,

 Blood glucose values, and intake and output.
 Urine is tested regularly for acetone.
 A record of daily weights is maintained,

.Promoting adequate nutrition

 Parenteral nutrition via a central line or enteral feedings administered via a nasogastric or
nasojejunal feeding tube may be used.

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  If there is discharge of csf from the nose (csf rhinorrhea), an oral feeding tube should be
inserted in Place of a nasal tube.
 Laboratory values should be monitored closely in patients receiving parenteral nutrition.
Elevating the head of the bed to prevent aspirating

Preventing injury

.Strategies to prevent injury include the following

• assess the patient to ensure that oxygenation is adequate and the bladder is not distended.
Check dressings and casts for constriction.

• to protect the patient from self-injury and dislodging of tubes, use padded side rails or wrap the
patient’s hands in mitts

.• avoid using opioids as a means of controlling restlessness because these medications depress
respiration, constrict the pupils, and alter responsiveness.

• minimize environmental stimuli by keeping the room quiet, limiting visitors, speaking calmly,
and providing frequent orientation

• provide adequate lighting to prevent visual hallucinations.

• minimize disruption of the patient’s sleep/wake cycles.

• lubricate the skin with oil or emollient lotion to prevent irritation due to rubbing against the
sheet.

• if incontinence occurs, consider use of an external sheath catheter on a male patient. Because
prolonged use of an indwelling catheter inevitably produces infection, the patient may be placed
on an intermittent catheterization schedule

Controlling temperature

Monitor temperature every 4 hours. If the temperature rises, efforts are Undertaken to identify
the cause and to control it using acetaminophen And cooling blankets .

If infection is suspected,potential sites of infection are cultured and antibiotics are prescribed
And administered.

Maintaining skin integrity

:• assess all body surfaces and document skin integrity at leastevery 8 hours.

• turn and reposition the patient every 2 hours.

• provide skin care every 4 hours.

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• assist patient to get out of bed to a chair three times a day If physically able.

Improving cognitive functioning

A neuropsychologist plans a program and initiates therapy or counseling to help the patient reach
maximal potential.

Cognitive rehabilitation activities help the patient to devise new problem-solving strategies.

Preventing sleep pattern disturbance

Environmental noise is decreased and the room lights are dimmed. Back rubs and other activities
to increase comfort can assist in promoting sleep and rest.

Supporting family coping

. Family counseling helps address the family members’ overwhelming feelings of loss and
Helplessness and gives them guidance for the management of inappropriate behaviors.

Support groups help the family members share problems, develop insight, gain information,
network, and Gain assistance in maintaining realistic expectations and hope.

CONCLUSION

Trauma involving the central nervous system can be life threatening.Even if not life-threatening,
brain and spinal cord injurymay result in major physical and psychological dysfunction and can
alter the patient’s life completely. Neurologic trauma affects the patient, the family, the health
care system, and societyas a whole because of its major sequelae and the costs of acuteand long-
term care of patients with trauma to the brain and spinal cord.

1.SUZANNE C. O’CONNELL SMELTZER,

BRUNNER & SUDDARTH’S
TEXTBOOK OF MEDICAL-SURGICAL NURSING
10TH EDITION
PAGE NO 1990-2010

2.BAILEY & LOVE’SSHORT

PRACTICE OF SURGERY
25THEDITION 2008
EDWARD ARNOLD (PUBLISHERS) LTD
PAGE NO 301-307

3.CHINTHAMANI
LEWIS MEDICAL SURGICAL NURSING
ELSEVIER PUBLICATION
1 ST EDITION
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Hypothermia for Intracranial Hypertension after Traumatic Brain Injury

Peter J.D. Andrews, M.D., M.B., Ch.B., H. Louise Sinclair, R.G.N., M.Sc., Aryelly
Rodriguez, M.Sc., Bridget A. Harris, R.G.N., Ph.D., Claire G. Battison, R.G.N., B.A.,
BACKGROUND
In patients with traumatic brain injury, hypothermia can reduce intracranial
hypertension. The benefit of hypothermia on functional outcome is unclear.
Full Text of Background...
METHODS
We randomly assigned adults with an intracranial pressure of more than 20 mm
Hg despite stage 1 treatments (including mechanical ventilation and sedation
management) to standard care (control group) or hypothermia (32 to 35°C) plus
standard care. In the control group, stage 2 treatments (e.g., osmotherapy) were
added as needed to control intracranial pressure. In the hypothermia group,
stage 2 treatments were added only if hypothermia failed to control intracranial
pressure. In both groups, stage 3 treatments (barbiturates and decompressive
craniectomy) were used if all stage 2 treatments failed to control intracranial
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 pressure. The primary outcome was the score on the Extended Glasgow
Outcome Scale (GOS-E; range, 1 to 8, with lower scores indicating a worse
functional outcome) at 6 months. The treatment effect was estimated with ordinal
logistic regression adjusted for prespecified prognostic factors and expressed as
a common odds ratio (with an odds ratio <1.0 favoring hypothermia).
Full Text of Methods...
RESULTS
We enrolled 387 patients at 47 centers in 18 countries from November 2009
through October 2014, at which time recruitment was suspended owing to safety
concerns. Stage 3 treatments were required to control intracranial pressure in
54% of the patients in the control group and in 44% of the patients in the
hypothermia group. The adjusted common odds ratio for the GOS-E score was
1.53 (95% confidence interval, 1.02 to 2.30; P=0.04), indicating a worse outcome
in the hypothermia group than in the control group. A favorable outcome (GOS-E
score of 5 to 8, indicating moderate disability or good recovery) occurred in 26%
of the patients in the hypothermia group and in 37% of the patients in the control
group (P=0.03).
Full Text of Results...
CONCLUSIONS
In patients with an intracranial pressure of more than 20 mm Hg after traumatic
brain injury, therapeutic hypothermia plus standard care to reduce intracranial
pressure did not result in outcomes better than those with standard care alone.
(Funded by the National Institute for Health Research Health Technology
Assessment program; Current Controlled Trials number, ISRCTN34555414.)
Very Early Administration of Progesterone for Acute Traumatic Brain Injury
David W. Wright, M.D., Sharon D. Yeatts, Ph.D., Robert Silbergleit, M.D., Yuko Y.
Palesch, Ph.D
BACKGROUND
Traumatic brain injury (TBI) is a major cause of death and disability worldwide.
Progesterone has been shown to improve neurologic outcome in multiple
experimental models and two early-phase trials involving patients with TBI.
Full Text of Background...
METHODS
We conducted a double-blind, multicenter clinical trial in which patients with
severe, moderate-to-severe, or moderate acute TBI (Glasgow Coma Scale score
of 4 to 12, on a scale from 3 to 15, with lower scores indicating a lower level of
consciousness) were randomly assigned to intravenous progesterone or placebo,
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 with the study treatment initiated within 4 hours after injury and administered for a
total of 96 hours. Efficacy was defined as an increase of 10 percentage points in
the proportion of patients with a favorable outcome, as determined with the use
of the stratified dichotomy of the Extended Glasgow Outcome Scale score at 6
months after injury. Secondary outcomes included mortality and the Disability
Rating Scale score.
Full Text of Methods...
RESULTS
A total of 882 of the planned sample of 1140 patients underwent randomization
before the trial was stopped for futility with respect to the primary outcome. The
study groups were similar with regard to baseline characteristics; the median age
of the patients was 35 years, 73.7% were men, 15.2% were black, and the mean
Injury Severity Score was 24.4 (on a scale from 0 to 75, with higher scores
indicating greater severity). The most frequent mechanism of injury was a motor
vehicle accident. There was no significant difference between the progesterone
group and the placebo group in the proportion of patients with a favorable
outcome (relative benefit of progesterone, 0.95; 95% confidence interval [CI],
0.85 to 1.06; P=0.35). Phlebitis or thrombophlebitis was more frequent in the
progesterone group than in the placebo group (relative risk, 3.03; CI, 1.96 to
4.66). There were no significant differences in the other prespecified safety
outcomes.
Full Text of Results...
CONCLUSIONS
This clinical trial did not show a benefit of progesterone over placebo in the
improvement of outcomes in patients with acute TBI. (Funded by the National
Institute of Neurological Disorders and Stroke and others; PROTECT III
ClinicalTrials.gov number, NCT00822900.)

An analysis of certain psychological tests used for the evaluation of brain injury.
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Armitage, S. G. (1946). An analysis of certain psychological tests used for the

evaluation of brain injury. Psychological Monographs, 60(1), i-48.

Abstract
Four tests previously used to determine the presence of brain injury were considered in
terms of their comparative advantages, disadvantages, and rationale. These tests were
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the Wechsler Mental Abilities Scale (Form B or MAS), Shipley-Hartford Retreat Scale
for Intellectual Impairment, Hunt-Minnesota Test for Organic Brain Damage, and
Rorschach Test. It is suggested that the Rorschach is the most useful for this purpose.
The brain injured group consisted of 44 patients who were known to have sustained
cerebral damage. The evidence was derived largely from surgeons' reports. In the
instances where these were lacking, positive pneumo-encephalograms and/or
neurological findings were available. The source of these injuries ranged from high
velocity missiles to auto accidents. In regard to the severity and type of injury the
neurologist distributed the 44 cases as follows: 11 severe, 21 moderate, and 12 mild; 9
were considered to have focal lesions, 17 were classed as focal-diffuse and 18 were
diffuse. The neurotics and normals do not appear to differ in any respect. Although this
was suggested by their means, it was considered best to make this test before the two
groups were combined into the control group and used averages have been affected by
the presence of a few extremely low or high scores. Four of the brain injured cases
during the free association period gave stories that bore little relationship to the one that
was read to them. However, they retained enough of the original story to receive some
credit. In every instance the confabulation had a central idea or theme and was fairly
coherent and cohesive, but in each instance elements of circumstantiality, preservation,
and pseudo-profundity were present. (PsycINFO Database Record (c) 2016 APA, all
rights reserved)

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