head injury , head injury nursing

1. HEAD INJURY
MRS. JISHA SRIVASTAVA
M.SC NURSING FIRST YEAR

2. IDENTIFICATION DATA

3. Mr. Anil Lioswami ,57 year old male was apparently normal till 13/1/2022. He is known old case
of Epilepsy. He is a chronic alcoholic and smoker since 15 years. He is also addicted to
tobacco chewing .On 14/1/2022 night he took excess alcohol and fall from stair at 9 pm. .He
was admitted to emergency Red zone at 10pm on 14/1/20221 in disoriented and unconscious
form with bleeding from head and mouth with a bp of 70/50mmhg and FAST negative. He was
breathless with a saturation of 88%. Since patient condition is deteoriated ,elective endo-
tracheal intubation done and shifted to ICU-103. During intubation bony fragments seen in
the mouth. He was shifted to ICU-103 on 14/1/22 at 11 Pm. Currently he is on ventilator support
connected via ET tube 8.5 Size. He is on MVI Mode with fio2 0.7, PEEP 6, Tidal Volume 450
ml ,Respiratory Rate 16/mt. He is afebrile and has tachycardia with HR 127 /mt. His BP is 112/70
mm of hg ,Spo2 is 98 %. He is attached to cardiac monitor. He is getting inj. Nomad 6 units in
50ml 5% dextrose. He has following lines and tube presently.
a.Right sublclavian line
b.18G canula on left hand
c.14 F folys catheter with urometer
3. HISTORY OF PRESENT ILLNESS

4. He is a known case of old case of Epilepsy. He is a chronic
alcoholic and smoker since 15 years. He is also addicted to
tobacco chewing.
No history of DM/TB / HTN /Cancer/ Allergy /Heart Disease/
Epilepsy / Mental Disorders
No history of any childhood diseases
No history of any previous hospitalisation.
5. PAST SURGICAL HISTORY
No history of past surgery or blood transfusion
4. PAST MEDICAL HISTORY

24. CONTENTS OF HEAD INJURY
➤ Introduction
➤ Anatomy and physiology of Nervous system
➤ Definition, Etiology
➤ Types of head injury
➤ Pathophysiology
➤ Clinical manifestations
➤ Diagnostic studies
➤ Prevention
➤ Emergency care, critical care
➤ Medical management, Surgical management
➤ Rehabilitation
➤ Nursing management
➤ Client education

25. INTRODUCTION
➤ The term traumatic head injury and traumatic brain
injury(TBI) injury are often used interchangeably in the
medical literature. This broad classification includes neuronal
injuries, haemorrhages, vascular injuries, cranial nerve injuries,
and subdural hygromas, and many others.

26. THE NERVOUS SYSTEM

27. PERIPHERAL NERVOUS SYSTEM(PNS):
The autonomic nervous system: Regulates events that are
automatic, or involuntary such as the activity of smooth muscles
and glands. The sub divisions are:
➤ Sympathetic (stimulates)
It is the “fight or flight” sub division which prepares the body
to cope with some threats
Its activation results in increase heart rate and blood pressure
➤ Parasympathetic (Inhibits)
It is the “housekeeping” system and is in control most of the
time
The division maintain homeostasis by seeing that normal
digestion and elimination occur and that energy is conserved

28. ➤ The somatic nervous system (SNS or voluntary nervous
system) is associated with the voluntary control of body
movements via skeletal muscles. It consists of :
➤ Sensory or Afferent division:
Consists of nerve fiber that consists of ascending tract ,carry
sensory information to the brain
➤ Motor or Efferent division: Carries impulses from the CNS
to effector organs, muscles and glands
PERIPHERAL NERVOUS SYSTEM(PNS):

29. The brain is located within the cranial cavity
of the skull and consists Cerebrum, diencephalon,
brain stem and cerebellum.
Cerebrum: The largest part of the brain and it is divided into
two hemispheres called the cerebral hemisphere.
Cerebrum contains four lobes:
➤ Frontal Lobe
➤ Reasoning
➤ Motor skills
➤ Cognition
➤ Emotions/ Personality
➤ Parietal Lobe
➤ Receives and process sensory information (pain, cold, touch etc.)
➤ Spatial relationship
➤ Temporal Lobe
➤ Hearing
➤ Memories
➤ Occipital Lobe
➤ Sight
THE BRAIN

37. •Hypothalamus: Regulates body temperature, hunger, hemostasis
•Thalamus: Relays sensory signal to and from the spinal cord
and cerebrum. Sensory input from the skin,viscera and special
sense organs is transmitted to the thalamus before
redistribution to the cerebrum.
•Pons: The pons is situated in front of the cerebellum,
below the mid brain and above the medulla oblongata.
It controls sleep as well as the rate and pattern of breathing.
•Medulla oblongata: It extends from the pons above and is continuous with the spinal
cord below.It is about 2.5cm long.Controls autonomic function,helps in regulation of
blood pressure, heart rate and breathing.
•Cerebellum: It is concerned with coordination of voluntary muscular movement,
coordination,posture and balance
MAJOR STRUCTURES:

39. The spinal cord is a cylindrical structure of nervous tissue,
composed of white and gray matter.
It extends from the foramen magnum where it is continuous with
the medulla to the level of the first or second lumbar vertebrae.
It is a vital link between the brain and the body, and from
the body to the brain.
The spinal cord is 40 to 50 cm long and 1 cm to 1.5 cm in
diameter.
Two consecutive rows of nerve roots emerge on each of its
sides. These nerve roots join distally to form 31 pairs of spinal
nerves.
It is uniformly organized and is divided into four regions: cervical
(C), thoracic (T), lumbar (L) and sacral (S).
THE SPINAL CORD

40. ➤ Gray matter: named for its pinkish-gray color, is home to neural cell bodies,
axon terminals, and dendrites, as well as all nerve synapses. This brain tissue
is abundant in the cerebellum, cerebrum, and brain stem. It also forms a
butterfly-shaped portion of the central spinal cord.The back portion of
this butterfly shape is known as the posterior, sometimes called the
dorsal gray horn. This region passes sensory information via ascending
nerve signals to the brain. The front part, which is sometimes called the
ventral gray horn, sends descending nerve signals governing motor
activities to autonomic nerves.
➤ white matter: of brain and spinal cord is composed of bundles of axons.
These axons are coated with myelin, a mixture of proteins and lipids, that
helps conduct nerve signals and protect the axons. White matter's job is to
conduct, process, and send nerve signals up and down the spinal cord
THE SPINAL CORD

42. Three layers of membranes known as
meninges protect the brain and spinal cord.
The delicate inner layer is the pia mater.
The middle layer is the arachnoid, a web-like
structure filled with fluid that cushions the
brain.
The tough outer layer is called the dura mater.
Cerebrospinal fluid is located in the
subarachnoid ,space between the arachnoid
mater and the pia mater.
The primary function of the meninges is to
protect the central nervous system.
MENINGES

43.
DEFINITION OF HEAD INJURY
➤ A break in the continuity of scalp,
skull bones, cranial blood
vessels or brain substance
is termed as head injury.

44. ➤ Gunshot wounds can cause head injuries .This can
damage the blood vessels and cause bleeding.
➤ Vehicle accidents are common causes of traumatic
head injuries.
➤ Violent shaking is a common cause of brain trauma in
infants and young children.
➤ Falling and hitting your head can damage the skull,
scalp, or brain.
➤ Assault can lead to a head injury. Being kicked,
punched, or struck in the head can cause a concussion,
closed or open brain injury.
ETIOLOGY

45. ➤ Occipital lobe
➤ Parietal lobe
➤ Frontal lobe
➤ Temporal lobe
➤ Brain stem
➤ Cerebellum
AREAS WHICH MOSTLY INVOLVED ARE:

46. Mechanisms contribute to head trauma are
1.Acceleration injury
2.Deceleration injury
3.Combination of acceleration and deceleration Injury
4. Deformation
MECHANISMS OF INJURY:

47. ➤ Acceleration injury: An acceleration injury
occurs when the immobile head is struck
by a ball. An example of this type of injury
is a client who is hit in the head with a baseball.
➤ Deceleration injury: If the head is moving
and hits an immobile object, a deceleration
type of injury seen in clients with trip fall,
hitting their head on furniture or wall.
MECHANISMS OF INJURY:

48. ➤ Combination of acceleration and deceleration injury:
Is occurs when the stationary head is hit
by a mobile objects and the head then
strikes the stationary surface. A soccer
player who sustains a blow to the head
and then hits the ground with his or her
head may sustain an acceleration,
deceleration injury.
➤ Deformation: Deformation refers to injuries
in which the force results in deformation and
disruption of the integrity of the impacted body
part ( e.g, skull fracture)
MECHANISMS OF INJURY:

49. Brain suffer to traumatic brain injury
Brain swelling and bleeding increase intracranial volume
Rigid cranium allows no room for expansion of
contents that lead increase ICP
PATHOPHISIOLOGY:

50. Pressure on blood vessels within the brain decrease blood supply to brain tissue
cerebral hypoxemia and ischemia occur
ICP continue to rise, brain may herniate or ceases blood flow
Cell death occurs, sometimes brain death
PATHOPHISIOLOGY:

51. TYPES OF INJURY
➤ BLUNT INJURY
➤ PENETRATING INJURY
➤ COUP AND COUNTERCOUP

52. ➤ BLUNT INJURY: Acceleration and
Deceleration injuries often results in
blunt trauma, involving several cranial
structures, including brain Parenchyma
and vessels. Because of brain
able to move within the skull ,movement
of the brain can result in injuries at
different locations.
TYPES OF INJURY

53. ➤ PENETRATING INJURY:
Penetrating Injuries include those made
by foreign bodies (e.g. knives and bullets )
those made by bone fragments from a skull
Fracture. Bone fragments from a skull fracture
cause local brain injury by lacerating brain
tissue and damaging other structures
(e.g. blood vessels ).
TYPES OF INJURY

54. ➤ COUP AND CONTRECOUP:
A coup injury occurs immediately at the
point of impact. Because of movement
within the skull, the same blow may cause
injury on the other side of the brain,
that is countercoup injury.
TYPES OF INJURY

55. Minor Brain injury : 13- 15, moderate brain injury : 9-12, Severe brain injury : 3- 8
COMPONENT RESPONSE SCORE
Eye response
Spontaneous
To speech
To pain
No response
4
3
2
1
Best Verbal Response
Oriented
Confused
Inappropriate words
Incomprehensible
sounds
None
5
4
3
2
1
Best Motor Response
Obeys commands
Localized pain
Flexion withdrawal
Abnormal flexion
Abnormal extension
No response
6
5
4
3
2
1
Total score
Best Response
Comatose patient
Totally unresponsive
15
8 or less
3
CLASSIFICATION ACCORDING TO GCS:

56. COMPONENT RESPONSE SCORE
Eye response
Eyelids open or opened, tracking
or blinking to command
Eyelids open but not tracking
Eyelids closed, but open to loud
voice
Eyelids closed, but open to pain
Eyelids remain closed to pain
4
3
2
1
0
Motor response
Thumbs up, fist or peace sign
Localizing to pain
Flexion response to pain
Extension response to pain
No response or generalized
myoclonus status
4
3
2
1
0
Brain stem
reflexes
Pupil and corneal reflexes present
One pupil wide and fixed
Pupil or corneal reflexes absent
Pupil and corneal reflexes absent
Absent pupil, corneal and cough
reflex
4
3
2
1
0
Respiration
Not intubated, regular breathing
pattern
Not intubated, Cheyne stokes
breathing pattern
Not intubated, irregular breathing
Breathes above ventilator rate
Breathes at ventilator rate or
apnea
4
3
2
1
0
CLASSIFICATION ACCORDING TO FOUR SCORE

57. ➤ PRIMARY INJURIES: Primary injury is an injury that results from the impact itself.
These are;
Scalp injuries
Skull fractures
Brain injuries
- Concussions
- Contusions
Diffuse axonal injury
➤ SECONDARY INJURIES: caused by hypoxia, hypercapnia, hypotension and
intracranial hypertension. The secondary problems occur hours to days after
the initial impact.
Epidural hematoma
Subdural hematoma
Acute and subacute subdural hematoma
Chronic subdural hematoma
Intracerebral hematoma
CLASSIFICATION : ACCORDING TO
STRUCTURE DAMAGE

58. ➤ SCALP INJURIES:
Scalp injuries are usually the result of direct
impact but may not be apparent in inflicted
injuries. Generally classified as minor injuries.
Trauma may result in;
➤ An abrasion (brush wound)
➤ Contusion
➤ Laceration
➤ Hematoma beneath tissue layers
Diagnostic findings:
➤ History
➤ Physical examination
➤ Inspection and palpation
➤ Major complications of scalp laceration are blood loss
and infection
PRIMARY INJURIES:

59. ➤ SKULL FRACTURE:
A skull fracture is a break in the continuity of the
skull caused by trauma. It may occur with or without
brain damage. The presence of a skull usually means
that there was a considerable force on impact. Skull
fractures classified as opened and closed. In an open
fracture, the dura is torn, and in closed fracture,
the dura is not torn.
➤ TYPES OF SKULL FRACTURE:
➤ Linear (Simple) - Break in continuity
➤ Comminuted - Multiple fracture line
➤ Depressed - bones of skull are forcefully
displaced downward
➤ Compound - skull fracture and scalp laceration with
communication to intracranial cavity.
PRIMARY INJURIES:

60. ACCORDING TO LOCATION OF SKULL FRACTURES:
➤ Frontal fracture
➤ Temporal fracture
➤ Parietal fracture
➤ Basilar skull fracture
➤ Orbital fracture
CLINICAL MANIFESTATIONS:
➤ Local injury
➤ Persistent pain usually suggest fracture
➤ May include cranial nerve deficits
➤ Battle’s sign – post auricular ecchymosis
➤ Raccoon eyes – periorbital ecchymosis
➤ Basilar fracture can extend up to paranasal sinus and middle ear
➤ Rhinorrhea or otorrhea confirms the involvement
➤ Rhinorrhea is also suggestive of post nasal sinus drainage.
➤ Haemorrhage from nose, pharynx or ear
COMPLICATIONS :
➤ Intra cranial infection, hematoma, meningeal and brain damage.
PRIMARY INJURIES:

61. BRAIN INJURY
Traumatic brain injury (TBI) encompasses a broad range
of pathologic injuries to the brain of varying clinical
severity that result from head trauma.
Even minor injury can cause significant brain damage,
irreversible brain damage and cell death occur when
blood supply is interrupted for only a few minutes, and
the damaged neurone cannot regenerate.

62. ➤ Open injury
➤ Closed injury
➤ Concussions
➤ Contusions
BRAIN INJURY

63. Open Injury:
➤ Open head injuries are those that penetrate the
skull. open brain injury occur when an object
penetrate the skull , enter the brain and damaged
soft brain tissue.
Closed Injury:
➤ Closed injuries are from blunt injury. It occurs when
the head accelerate and then rapidly decelerate
with another object and the brain tissue is damage
but there is no opening through the skull and dura
BRAIN INJURY

64. Concussions:
Concussion is a temporary loss of neurological
function with normal brain structure. A concussion
is a head trauma that may result in loss of consciousness
5 minute or less and retrograde amnesia. There is no
break in the skull, dura and no damage is visible
in CT and MRI scan.
Clinical Manifestations:
➤ Headache
➤ Dizziness
➤ Nausea and vomiting
➤ Difficulty in speaking
➤ Difficulty in awakening
➤ Confusion
➤ Weakness of one side of the body
BRAIN INJURY

65. ➤ Contusions:
Contusion damage the brain substance itself,
causing multiple areas of petechial and
puncture haemorrhage. Abnormalities may
be mainly in one part of the brain, but
other areas may also be injured.
Contusions may be divided into
cerebral contusion and brain stem contusion
BRAIN INJURY

66. ➤ Cerebral contusion: Manifestations of cerebral contusions vary
depending on which areas of the hemispheres are damaged.
➤ An agitated, confused head injured client who remains
alert may have a temporal lobe contusion.
➤ Hemiparesis in an alert head injured client may indicate
a frontal contusion.
➤ An aphasic head injured client may have a
frontotemporal contusion.
➤
BRAIN INJURY

67. Brain stem contusion: Brain stem contusion render a client
immediately unresponsive or partially comatose because of significant
brain stem disruption. The patient may lie motionless
➤ Pulse is feeble
➤ Shallow respiration
➤ Skin cold and pale
➤ Sub normal temperature and blood pressure
➤ Abnormal motor function
➤ Elevated ICP
BRAIN INJURY

68. Diffuse axonal injury is most severe form of brain
injury. In this damage of axons in the cerebral
hemispheres, corpus callosum and brain stem
occurs. Diffuse axonal injury may be classified
as mild, moderate, severe.
➤ Mild diffuse axonal injury consists of loss
of consciousness lasting 6 to 24 hours.
➤ Moderate diffuse axonal injury is coma less
than 24 hours with incomplete recovery on
awakening
➤ Severe diffuse axonal injury includes
primary injury to the brain stem, it begins with
immediate loss of consciousness, prolonged
coma, abnormal flexion, extension, posturing,
increased ICP, hypertension and fever.
DIFFUSE AXONAL INJURY:

69. ➤ Secondary injuries are complications of initial injury.
EPIDURAL HAEMATOMA :
➤ An epidural haematoma, also called
an extradural haematoma, form
between skull and dura matter.
Bleeding is almost always continuous,
and large clots formed which separates
the dura from the skull.
SECONDARY INJURIES:

70. ➤ SUBDURAL HAEMATOMA
➤ Collection of blood between dura matter
and the brain caused by coagulopathies and
rupture of an aneurysm, bleeding is venous in origin.
Further classified as:
➤ Acute - Symptoms developed within 24 – 48 hours
➤ Subacute - within 24 to 2 weeks
➤ Chronic - within 3weeks to months
SECONDARY INJURIES:

71. CLINICAL MANIFESTATIONS
➤ Deteriorating neurological state raises the
possibility of a subdural haematoma
➤ Irritable and confused
➤ Coma
➤ Loss of consciousness
➤ Increased ICP
➤ Hemiparesis
➤ Pupillary dilatation
➤ Extraocular eye movement paralysis.

72. ➤ CHRONIC SUBDURAL HAEMATOMA
➤Chronic subdural haematoma involves two groups:
• Who has suffered a significant and often severe head injury
• Non traumatic group with rupture of fragile bridging vein in
atrophic ‘mobile’ brain.
➤Clinical manifestations:
• Raised ICP without localizing signs
• Headache, vomiting
• Fluctuating drowsiness
• Inattentive and incoherent
• A progressive dementia
• May develop neurologic signs
• Hemiparesis

73. INTRACEREBRAL HAEMATOMA
➤ Bleeding directly into the brain tissue
and may occur at the area of injury,
some distance or deep within the brain
Clinical manifestations:
➤ Assessment findings are similar
to other two, but hemiplegia is
more common.

74. GENERAL APPROACH TO HEAD INJURY
Clinical manifestations:
❖ Disturbances of consciousness
❖ Confusion
❖ Pupillary abnormalities
❖ Sudden onset of neurologic deficits
❖ Changes in vital signs
❖ Visual and hearing impairment
❖ Sexual dysfunction
❖ Spasticity
❖ Headache
❖ Vertigo
❖ Movement disorders
❖ Seizures
❖ Hypovolemic shock suggests
possibility of multisystem injury

75. DIAGNOSTIC EVALUATION
Laboratory studies:
➤ Sodium levels: hyponatremia may be due to the syndrome of
inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting;
elevated sodium levels in head injury indicate simple dehydration or
diabetes insipidus.
➤ Magnesium levels: These are depleted in the acute phases of minor and
severe head injuries.
➤ Coagulation studies: Including prothrombin time (PT), activated partial
thromboplastin time (aPTT), and platelet count
➤ Blood alcohol levels and drug screens: May help to explain subnormal
levels of consciousness and cognition in some patients with head trauma.
➤ Renal function tests and creatinine kinase levels: To help exclude
rhabdomyolysis if a crush injury has occurred or marked rigidity is present.
➤ Neuron-specific enolase and protein S-100 B: Elevated serum levels may
correlate with persistent cognitive impairment at 6 months in patients with
severe or mild head injuries.

76. Imaging studies:
I.) Electroencephalography: The most useful role of
electroencephalography (EEG) in head injuries may be to
assist in the diagnosis of non-convulsive status epilepticus.
II.) MRI and CAT Scans: The MRI does with magnetic fields; the
CAT scan uses x-rays. The
MRI provides more detail than the CAT scan. Hence, brain
damage seen on an MRI –as small as 1-2mm in size - may
escape detection by a CAT scan.
The CAT scan is superior to the MRI in detecting fresh blood
in and around the brain, while the MRI is better at detecting
the remnants of old hemorrhaged blood, called
hemosiderin.
DIAGNOSTIC EVALUATION

77. 3.) Computed Tomography Scan (also called a CT or CAT scan ): A diagnosticimaging
procedure that uses a combination of X- rays and computer technology to produce
horizontal, or axial images (often called slices) of the body . A CT scan shows detailed
images of any part of the body, including the bones, muscles, fats and organs.
4.) Angiography: Once a common diagnostic study in persons with acute head injury,
angiography is rarely used in the evaluation of acute head injury today. However,
conventional angiography has been the screening and diagnostic modality of choice
for identifying blunt cerebrovascular injuries (BCVI) in trauma patients. Angiography is
used in acute head injury only when a vascular injury may be present. This includes
patients with unexplained neurologic deficits, especially in the setting of temporal
bone fractures, and patients with clinical evidence of a potential carotid injury
(e.g., hemiparesis, Horner syndrome.)
DIAGNOSTIC EVALUATION

78. MANAGEMENT
LEVELS OF PREVENTION
➤ Primary prevention:
• Teach the client to use safety restrains in cars and to
wear bicycle helmets, and roller blade helmet
• Instruct clients not to drive after drug or alcohol ingestion.
➤ Secondary prevention:
• Help the client to control pre – existing conditions that
may affect recovery from injury.
➤ Tertiary prevention:
•Stabilize and transport the client to a tertiary care

79. DO’S AND DON’T
DO’S:
❖ If bleeding profusely, apply pressure (if no fracture)
❖ If the client is vomiting, roll him as a log
❖ If eyes are swollen, apply cold compress
❖ Take to hospital if becomes drowsy, develops headache and
stiffness of neck,demonstrates behavioral abnormalities
DON’T:
❖ Wash a wound which is deep and bleeding
❖ Remove any object sticking out of the wound
❖ Move the patient unless absolutely necessary
❖ Remove the helmet if serious injury
❖ Pick up a child with sign of the severe injury

80. CRITICAL CARE/ACUTE CARE MANAGEMENT
This is the “platinum 10 minutes” and the “golden hour” of
intervention.
AIMS OF MANAGEMENT IN ACUTE STAGE:
➢ To stabilize the patient
➢ To protect from further injury
➢ To rule out spinal injury
➢ To manage intracranial pressure

81. GCS < 8 with ICP > 22mmhg
Secure airway and ensure adequate ventilation
Sedation and analgesia in intubated patient
Neuromuscular blocking drugs if required
Ensure PACO2 between 35 – 40 mmhg
External ventricular drain to allow intermittent CSF drainage
Brief period of hyperventilation if ICP is sustained > 22 mmhg
CRITICAL CARE/ACUTE CARE MANAGEMENT

82. Mannitol (20%) in a dose of 0.25 – 1.0 gm/kg
Or
Hypertonic saline (3%) in a dose of 3 -5 cc/kg
Depressive craniectomy
Barbiturate or propofol coma may be induced for patients
who have failed to respond to above measures.
Moderate hypothermia ( 33 – 34°C ) may be used
CRITICAL CARE/ACUTE CARE MANAGEMENT

83. ➤ Airway maintenance: With cervical spine control, any head
injured patient with a Glasgow coma scale less than 8 should
be intubated. A rapid sequence technique is recommended,
an anaesthetic drugs (for e.g., thiopental or propofol for
induction with suxamethonium for muscle relaxation) must be
used to avoid fatal increases in intracranial pressure (ICP).
➤ Breathing or ventilation: must be optimized to “low
normocapnia”, that is arterial partial pressure of carbon
dioxide ( PACO2 ) of of 4 – 4.5 kpa .Hyperventilation to lower
PACO2 levels .An arterial partial pressure of oxygen (PAO2)
greater than 13 kpa should be maintained. Until arterial blood
gases can be measured, non – invasive monitoring with a
pulse oximeter and capnography is recommended.
CRITICAL CARE/ACUTE CARE MANAGEMENT

84. ➤ Circulation: is maintained by fluids and inotropes to maintain a mean
arterial blood pressure of 90 mmHg. The primary aim in the resuscitation
of a patient with brain injury with or without trauma is the maintenance
of euvolemia.
➤ Maintaining CPP(Cerebral perfusion pressure): After brain injury, and
especially in the multiple injured patient,
cerebral blood flow may be lowered to the ischemic threshold. To
prevent further
neuronal death (secondary brain injury), the flow of well oxygenated
blood must be restored. There is no class 1 evidence for the optimum
level of CPP, but 70 – 80 mmHg is probably the critical threshold.
Therefore, maintenance of a mean arterial pressure of 90 mm Hg is
usually recommended.
CRITICAL CARE/ACUTE CARE MANAGEMENT

85. OSMOTHERAPY AND MAINTAINING ICP:
➤ Osmotherapy has been used since the first published use of mannitol to treat raise
ICP. Mannitol remains the standard against which other ICP lowering fluids are
compared. The usual dose in which mannitol is recommended is 0.5 – 1g/kg.
HYPERTONIC SALINE:
➤ Currently, the most researched area has been the use of hypertonic saline. This is an
age where it is already being used therapeutically. It has become quiet clear that it
is effective in concentrations of 3 – 7.5% in lowering ICP.
BARBITURATES:
➤ High dose barbiturate therapy is usually reserved for refractory intracranial
hypertension on patients who are felt to be salvageable. They exert a beneficial
effect by lowering the cerebral metabolic rate for oxygen and modulating vascular
tone. They also have additional effects such as membrane stabilization.
CRITICAL CARE/ACUTE CARE MANAGEMENT

86. Temperature control:
➤ Hypothermia has been shown to be neuroprotective in
many TBI models. Several mechanisms for this have been
postulated, including decrease excitatory amino acids in
the injured area, augmenting antioxidant activity, and
reducing inflammatory markers.
➤ Our clinical practice is to monitor core temperature
regularly and prevent its rise by using antipyretic agents.
Systemic infections contributing to pyrexia are identified
and treated aggressively.
CRITICAL CARE/ACUTE CARE MANAGEMENT

87. OTHER SUPPORTIVE TREATMENTS
➤ Early extra ventricular drainage of CSF is sometimes of
value in controlling brain edema .
➤ Neuromuscular paralysis may decrease ICP by
preventing sudden changes related to coughing or
straining and by promoting systemic venous pooling that
increases venous drainage from the head.
➤ Trying to differentiate a drug – induced coma from an
increased ICP – induced coma with trial of Naloxone
(Narcan)is contraindicated, as it is invariably induces
agitation, If the stupor is narcotic induced.

88. ➤ Use of positive end – expiratory pressure (PEEP) for mechanical
ventilation is controversial in TBI patients with acute lung injury/
acute respiratory distress syndrome. Zhang has found that PEEP
can have a varied impact on blood, intracranial and cerebral
perfuse pressure in patients with cerebral injury. When applying
this technique, mean and intracranial pressure monitoring
appears beneficial.
➤ The patient may need surgeries for injuries. In addition to the
trauma surgeon, a surgical staff could include the neurosurgeon,
a physician who performs brain and spinal cord surgery, an
orthopedic surgeon, a physician who works with broken bones
such as fractures of the arms and legs or the spinal column, or a
general surgery.
OTHER SUPPORTIVE TREATMENTS

89. MEDICAL MANAGEMENT
The medical management of severely head injured clients focuses on supporting all
organ systems while recovery from the injuries takes place.
VENTILATORY SUPPORT:
➤ Ventilations of patients with severe TBI aims to maintain PCO2 within a normal
range of 34 – 38 mm Hg. Hypoventilation should be avoided, as increased PCO2
level may lead to cerebral hyperemia with an increase in blood volume and ICP.
Hyperventilation on the other hand, results in an increased risk of vasoconstriction
and increased tissue hypoxia, especially in the penumbra zone, so it is best
avoided. The ongoing EPIC trial in Arizona focuses on avoidance of
hyperventilation in TBI patients in a prehospital setting because it may lead to an
approximately mix – fold increase in poor outcomes. Hyperventilation up to a
Paco2 of 25 mmHg for the purpose of reducing ICP is still accepted.

90. ➤ MAINTAINING ICP AND CPP:
Vasopressors are commonly used to augment CPP in the
setting of TBI.
1.Maintaining SBP >100 mm Hg for patients 50 to 69 years old
or at > 110 mmHg or above for patients 15 to 49 or over 70
years old to decrease mortality and improve outcomes .
2.The recommended target CPP value for survival and
favorable outcomes is between 60 and 70 mmHg. Whether 60
or 70 mmHg is the minimum optimal CPP threshold is unclear
and may depend upon the patient’s auto regulatory status.
3.Avoiding aggressive attempts to maintain CPP above 70
mmHg with fluids and pressors may be considered.
MEDICAL MANAGEMENT

91. ➤ FLUID MANAGEMENT:
➤ In a hypotensive TBI patient, hypovolemia resulting from
extracranial haemorrhage should be first ruled out. Even
in the absence of extracranial haemorrhage,
hypovolemia can still develop by trans capillary leakage.
➤ Crystalloids are usually poor volume expanders, as 70 –
80% reaches the interstitial space within 20 minutes of
infusion, contributing to general systemic tissue edema.
Saline is the most common crystalloid used in TBI patients.
MEDICAL MANAGEMENT

92. ➤ SEDATION AND ANALGESICS:
➤ Reducing stress and the adrenocortical response is an important component of
TBI management. Even unconscious TBI patients may have increased blood
pressure and ICP resulting from this stress response.
➤ Achieving an adequate level of sedation is paramount because it minimizes
the length of hospital stay, ventilator days, incidence of delirium and helps in
early mobilization.
➤ The latest BTF(Brain trauma foundation) recommendations regarding the use of
sedatives and analgesics are as follows:
1.Administration of barbiturates to induce burst suppression as prophylaxis against
intracranial hypertension is not recommended .
2.High dose barbiturates are recommended to control ICP refractory to maximum
standard surgical and medical treatments while ensuring hemodynamic stability.
3.Propofol (Inhibits GABA -A )may be used for ICP control.
MEDICAL MANAGEMENT

93. OSMOTHERAPY:
➤ Osmotherapy with mannitol has been used since 1960’s as
the main treatment for raised ICP and remains a component of TBI
management guidelines.
➤ Hypotonic saline has become an alternative
during the last 20 years, but controversy remains regarding which
solution is the best agent and regarding the best method of
administration.
➤ Mannitol increases Cerebral blood flow by plasma expansion,
decreasing the blood viscosity via deformed erythrocytes, and
promoting osmotic diuresis. Hypertonic saline promotes the flux of
water across the BBB(Blood brain barrier) and improved blood flow and
expanding the
plasma volume
MEDICAL MANAGEMENT

94. GLYCEMIC CONTROL:
➤ After TBI there is a marked catecholamine surge, with cortisol
release and glucose intolerance leading to significant
hyperglycemia.
➤ Anaerobic metabolism of glucose and resulting acidosis in the
brain may lead to neuronal dysfunction and cerebral oedema.
Impaired
➤ cerebrovascular regulation following TBI has also been implicated
as a reason for poor outcome because of hyperglycemia.
➤ Glucose – containing fluids should be avoided and blood sugar
monitored to maintain levels between 4-8mmol/L(upto 140mg/dl).
MEDICAL MANAGEMENT

95. NUTRITIONAL MANAGEMENT
➤Early nutritional support is associated with better outcomes
and enteral feeding has been found to be beneficial.
➤Basal caloric replacement by at least the fifth day, and at
most by the seventh day post – injury.
➤Trans gastric jejunal feeding may also reduce the risk of
ventilator associated pneumonia.
➤Patients with severe TBI have gastric feeding intolerance,
which may be attributed to dysfunctional gastric emptying
secondary to increased ICP and use of opiates.
➤Prokinetic agents, such as metoclopramide, may improve
feeding tolerance.

96. CHRONIC MANAGEMENT
SYMPTOM
PHARMACOLOGIC
TREATMENT
REFERRAL AFTER POOR
RESPONSE TO TREATMENT
Anxiety
Anxiolytic drugs (short
term),SSRI
Mental health referral,
social support
Cognitive problems
(e.g. trouble with
concentration, memory
and decision making)
Consider
pharmacologic
treatment after ruling
out sleep disorders,
SSRIs
Consider referral to
mental health services,
cognitive rehabilitation
or traumatic brain injury
specialist.
Emotional problems
(e.g. depression,
irritability, poor
frustration tolerance)
Antiepileptic drugs,
SSRIs
Mental health referral,
social support
Fatigue( e.g. Loss of
energy, easily tired)
Consider
pharmacologic
treatment after ruling
Mental health referral

97. SYMPTOM
PHARMACOLOGI
C TREATMENT
NON –
PHARMACOLOGIC
TREATMENT
REFERRAL
CONSIFDERATIONS
IF NO RESPONSE TO
Change in
appetite
Consider mental
health referral
Dizziness
Antibiotics,
decongestant
s for middle
ENT referral,
neurology referra
after ENT
Headache
Non –
narcotic
analgesics,
Non-steroidal
Sleep hygiene
education, physical
therapy, relaxation
Neurology
referral, pain
clinic
Hearing
problems
( e.g.
Environmental
modifications.
Audiology or ENT
referral, Speech
and language
Nausea Antiemetics
Sleep hygiene
education
Gastroenterology
referral
Sleep
disturbances
Sleep
medications
Sleep hygiene
education
Mental health,
neurology or
physical
Vision
Problems
Sleep hygiene
education, light
Optometry or
Ophthalmology

98. SURGICAL MANAGEMENT
➤ Decompressive craniectomy
(DC)are noted as life saving
procedures to prevent further
compounding secondary injuries
and central herniation. DC’s are
considered for diffused brain
injury vs focal extra – axial or
parenchymal injury.

99. ACUTE EPIDURAL HAEMATOMA (EDH)
The classic presentation of an acute EDH is a loss
of consciousness followed by a lucid interval and
obtundation in sequence, and a lens Shaped
haemorrhage on CT. The source of this haemorrhage
is typically the middle meningeal artery, however,
bleeding may occur from a sinus or the bone itself in
the setting of a skull fracture. Indications for operative
management are based on imaging and patient status.
A volume greater than 30 cc should be evacuated
regardless of GCS. If the decision to proceed to the
OR is made, it should be done as soon as possible
especially in the setting of GCS <9 or anisocoria. A
craniotomy, does provide more complete haematoma
evacuation.
SURGICAL MANAGEMENT

100. ACUTE SUBDURAL HAEMORRHAGE (SDH):
For patients presenting with an acute SDH the
generally accepted indications for surgery is
a thickness greater than 10mmHg and midline
shift greater than 5mm on the CT scan. It is
recommended that patients presenting with
these findings be operated on regardless of
their GCS. If the ICP rise to greater than 20 mmHg
or if abnormal pupillary responses are observed,
surgery is recommended. If the decision to proceed to
surgery is made, the timing should be emergent.
The preferred method is a craniotomy with or
without bone flap removal or duroplasty
depending on intraoperative findings.
SURGICAL MANAGEMENT

101. TRAUMATIC PARENCHYMAL LESION:
Indication for surgery in this type of injury is
an intracerebral lesion with neurological deterioration,
and intracranial hypertension that is not responsive to
medical management or signs of mass effect on CT.
Furthermore, patients with a GCS less than 9 and a
frontal or temporal lesion, with volume greater than
20 cc with midline shift greater than 5mm or cisternal
compression or any lesion volume greater than 50 cc
may be considered for evacuation. . The timing of
proceeding to the OR should be emergent. A craniotomy
is generally recommended . If the patient is suffering from
medically refractory intracranial hypertension, a bifrontal
decompressive craniectomy (DC) may be considered.
Other options for decompression include a temporal
lobectomy, hemispheric DC and subtemporal decompression.
SURGICAL MANAGEMENT

102. DEPRESSED CRANIAL FRACTURES:
Indication for surgery include open skull fractures depressed
to a degree greater than the thickness of the skull. These should
be operated on to prevent infection and further damage to
underlying brain parenchyma. If the decision to proceed to the
operating room is made, it should be done in a timely fashion.
Methods for repaired include elevation of bone flap and
debridement of the overlying tissue. Foreign objects if present
should be removed and copious irrigation performed.
If the fracture is open, complex and comminuted, the
fracture cranium may be removed and the defect may
be repaired later to help preventing subsequent infection.
If the wound has no signs of gross contamination or infection,
or if it was a closed fracture, using the original bone flap is an option.
SURGICAL MANAGEMENT

103. PENETRATING TRAUMA:
The primary indication for surgery is control of ICPs and
secondary injury, but the removal of the penetrating
foreign object may be considered. The injury itself most
often includes the overlying skin,skull, dura, parenchyma,
ventricles cisterns and vascular structures. Great care must
be made to determine the involvement of each of these
structures in order to surgically manage the patients.
SURGICAL MANAGEMENT

104. COMPLICATIONS:
•Cerebral edema
•Infection
•Acute hydrocephalus
•Syndrome of inappropriate secretion
of diuretic hormone
•Neurogenic pulmonary edema
•Arteriovenous aneurysms
•Altered behavior
•Diabetes insipidus

105. DISCHARGE AND FOLLOW UP
➤ Give verbal and printed discharge advice to patients with any degree of
head injury who are discharged from an emergency department or
observation ward, and their families and caregivers.
➤ Printed advice for patients, family members and care givers should be
age appropriate and includes:
❖ Details of the nature and severity of the injury
❖ Risk factors that mean patients need to return to the emergency
department
❖ A specification that a responsible adult should stay with the patient for the
first 24 hours after their injury
❖ Details about the recovery process, including the fact that some patients
may appear to make a quick recovery but later experience difficulties or
complications.
❖ Contact details of community and hospital services in case of delayed
complications.
❖ Information about return to everyday activities, including school, work,
sports and driving.

106. REHABILITATION CENTRE
➤ Rehabilitation is a treatment or treatments designed to facilitate the
process of recovery from injury, illness, or disease to as normal a
condition as possible.
➤ GOALS:
▪ Stabilize the medical and rehabilitation issues related to brain injury
and other injuries.
▪ Preventing secondary complications. Complications could include
pressure sores, pneumonia and contractures.
▪ Restore lost functional abilities. Functional changes could include
limited ability to move, use the bathroom, talk, eat and think.
▪ The staff will also provide adaptive devices or strategies to enhance
functional independence.
▪ The staff will begin to analyze with the family and the patient what
changes might be required when the person goes home.

107. REHABILITATION TEAM
➢ Physiatrist
➢ Occupational therapist
➢ Physical therapist
➢ Speech and language pathologist
➢ Neuropsychologist
➢ Social worker or case manager
➢ Rehabilitation nurse
➢ Traumatic brain injury nurse specialist
➢ Vocational counselor

108. ➤ Assessment:
It may be necessary to wake up a head injured patient hourly for assessment
during the first 24 to 48 hours after injury. Parameters assessed includes the
following;
LOC and apprehension
Pupillary size, direct responses to light and ocular movement.
Vital signs – Blood pressure, temperature, pulse rate and quality, respiratory rate
and quality.
Motor strength
Speech
Vision
Reaction to auditory and painful stimuli
Response to command
Spontaneous activity
General response to stimulation
NURSING MANAGEMENT:

109. NURSING DIAGNOSIS
1. Ineffective airway clearance related to coma or bleeding in airway
Interventions:
➤ Maintain patent airway, remove foreign body from mouth and
oropharynx
➤ Assess respiratory rate , rhythm and chest expansion.
➤ Suctioning the oropharynx and trachea every 1 – 2 hourly
➤ Provide semi prone or lateral position if not contraindicated
➤ Repositioning the patient every 2 hours helps to mobilize pulmonary
secretions and prevent stasis with the help of the bed elevated
about 30 degrees to decrease intracranial venous pressure.
➤ Administer humidified oxygen as per doctor’s order
➤ Closely monitoring arterial blood gas values to assess the adequacy
of ventilation
➤ Maintain Pao2 by endotracheal intubation, a tracheostomy or a
mechanical ventilator, if required

110. 2.Altered cerebral tissue perfusion related to hypotension,
intracerebral haemorrhage, haematoma or other injury.
Interventions:
➤ Assess level of consciousness, pupillary response, cognitive functions every 1 – 4 hourly
➤ Response to verbal commands, withdraw to pain every 1 – 4 hourly
➤ Monitor vitals, pulmonary and cardiovascular status
➤ Monitor intake and output every 1 – 4 hourly
➤ Elevate head end of the bed 30 degree and keeping the head in neutral position
➤ Avoid extreme hip flexion
➤ Monitor ECG
➤ Assess signs of bleeding in abdomen , chest and pelvis
➤ Check for haematuria
➤ Administer blood and blood products as per doctor’s order if required
➤ Report, record and assess more frequently if any deterioration is evident
NURSING DIAGNOSIS

111. 3.Fluid volume deficit related to disturbances of
consciousness and hormonal dysfunction
Interventions:
➤ Asses the signs of dehydration, electrolyte imbalance
and uremia
➤ Monitor electrolytes, blood glucose level, blood urea
nitrogen, urine specific gravity and urine acetone
➤ Maintain intake and output chart
➤ Monitor daily weight
➤ Fluid replacement as per doctor’s ordered, if required
NURSING DIAGNOSIS

112. 4.Altered urinary elimination pattern related to lack of
awareness of bladder distension, unconsciousness
Interventions:
➤ Assess intake and output every 4 hourly
➤ Assess for urinary retention, overflow and incontinence
➤ Intermittent catheterisation preferred to indwelling
catheter
➤ Bladder training program as soon as possible
➤ Monitor daily for signs of urinary tract infection.
NURSING DIAGNOSIS

113. 5.Altered bowel elimination pattern related to loss of
muscle tone, reflexes and inactivity.
Interventions:
➤ Auscultate bowel sounds in every shift
➤ Check for stool impaction daily
➤ Administer stool softeners, laxatives, suppositories, or
enemas as needed
➤ Add water to diet
➤ Advise to take fiber rich diet
NURSING DIAGNOSIS

114.
6. SELF CARE DEFICIT RELATED TO DECREASE LOC
Interventions:
➤ Assess the conscious level of the patient
➤ Assess the activities level of the patient
➤ Activities should be spaced to allow for rest, because
clustered activities may increase ICP
➤ Assist the client while doing activities
NURSING DIAGNOSIS

115. 7. SLEEP PATTERN DISTURBANCES RELATED TO FREQUENT ASSESSMENTS AND RESTLESSNESS
Interventions:
➤ Assess the sleeping pattern of the patient
➤ Provide emotional support
➤ Allow minimum visitors
➤ Provide quiet, cool and calm environment
➤ Administer sedatives as per doctor’s order if required
NURSING DIAGNOSIS

116. 8.HIGH RISK FOR SEIZURES RELATED TO BRAIN INJURY, HYPOXIA,
ELECTROLYTE IMBALANCE AND FLUID VOLUME ALTERATION
Interventions:
➤ Protect from injury
➤ Check for adequate airway, don’t force a tongue blade
into mouth
➤ Observe onset, progression, duration of seizure
➤ Monitor vitals, suction SOS and monitor onset status
epilepticus
➤ Monitor serum electrolyte
➤ Administer antiepileptic as order
NURSING DIAGNOSIS

117. 9.RISK FOR IMPAIRED SKIN INTEGRITY RELATED TO IMMOBILITY BED REST, HEMIPARESIS,
HEMIPLEGIA AND LACK OF AWARENESS ABOUT TURN.
Intervention:
➤ Assessing all body surfaces and documenting skin integrity
every 8 hours.
➤ Turning and repositioning the patient every 2 hours.
➤ Providing skin care every 4 hours.
➤ Assisting the patient to get out of a bed to wheelchair (unless
contraindicated).
➤ Lubricating the skin with oil or emollient lotion to prevent
irritation and skin breakdown due to rubbing against the
sheet.
➤ Provide back care
NURSING DIAGNOSIS

118. 10. ALTERED THOUGHT PROCESSES RELATED TO MEMORY DEFICIT, ALTERED LOC,
IMPAIRED REASONING ABILITY, CONFUSION
➤ Assess the LOC
➤ Orientate to person, time and place daily
➤ Explain all nursing activities before initiating
➤ Use alternatives methods of communication as needed
➤ Use low bed with side rails
➤ Consult with rehabilitation therapists
➤ Involve client and family members in care planning
and goal setting.
NURSING DIAGNOSIS
Interventions

119. CLIENT EDUCATION:
Observe for 24 hours after injury. Take him/her to the hospital
immediately if any of the following occurs:
➤ Increased drowsiness and confusion
➤ Inability to be awakened
➤ Vomiting
➤ Convulsions
➤ Bleeding or drainage from nose or ears
➤ Weakness in either arm /leg
➤ Blurring of vision
➤ Slurring of speech
➤ Enlargement or shrinkage of one pupil.
➤ Worsening headache or stiff neck
➤ Behavioral changes (e.g. irritability, anger)

120. CONCLUSION
➤ Head injury is a devastating injury and often these
patients would require monitoring and treatment in ICU.
Management requires multidisciplinary approach,
frequent close monitoring and judicious use of multiple
treatment to lessen secondary brain injury and improve
outcomes.

121. SUMMARIZATION
➤ Anatomy and physiology of Brain
➤ Definition, Etiology
➤ types of head injury,
➤ pathophysiology,
➤ clinical manifestations,
➤ Diagnostic studies,
➤ Prevention,
➤ Emergency care, critical care
➤ Medical management, Surgical management,
➤ Rehabilitation,
➤ Nursing management
➤ Client education.

122. RESEARCH JOURNAL
Comparison of Cognitive Behavioral Therapy and Supportive Psychotherapy for
the Treatment of Depression Following Traumatic Brain Injury: A Randomized
Controlled Trial Ashman, Teresa PhD; Cantor, et.al
Objective:
➤ To determine the efficacy of 2 different interventions (cognitive behavioral
therapy [CBT] and supportive psychotherapy [SPT]) to treat post-traumatic
brain injury (TBI) depression.
Participants:
➤ A sample of 77 community-dwelling individuals with a TBI, and a diagnosis of
depression. Participants were randomized into treatment conditions either
CBT or SPT and received up to 16 sessions of individual psychotherapy.
Measures:
➤ Participants completed the Structured Clinical Interview for DSM-IV and self-
report measures of depression (Beck Depression Inventory-Second Edition),
anxiety (State-Trait Anxiety Inventory), perceived social support (Interpersonal
Support Evaluation List), stressful life events (Life Experiences Survey), and
quality of life (QOL) before beginning and immediately following treatment

123. RESULTS:
➤ No significant differences were found at baseline between CBT and SPT groups
on demographic factors (sex, age, education, race, and time since injury) or
baseline measures of depression, anxiety, participation, perceived social
support, stressful life events, or QOL. Analyses of variance revealed significant
time effects for the Beck Depression Inventory-Second Edition, State-Trait
Anxiety Inventory, and QOL outcome measures but no group effects. Intention-
to-treat mixed effects analyses did not find any significant difference in
patterns of scores of the outcome measures between the CBT and SPT
intervention groups.
CONCLUSIONS:
➤ Both forms of psychotherapy were efficacious in improving diagnoses of
depression and anxiety and reducing depressive symptoms. These findings
suggest that in this sample of individuals with TBI, CBT was not more effective in
treating depression than SPT, though further research is needed with larger
sample sizes to identify different components of these interventions that may
be effective with different TBI populations.
RESEARCH JOURNAL

124. ➤ Fatigue and Sleep Disturbance Following Traumatic Brain Injury—
Their Nature,
Causes, and Potential Treatments. Ponsford, Jennie L. PhD; Ziino, et.al
➤ Abstract
Background:
Although fatigue and sleep disturbance are commonly reported
following
traumatic brain injury (TBI), understanding of their nature and
treatment remains
limited.
➤ Objectives:
This article reviews a series of investigations of the nature and causes of
fatigue and
sleep disturbance following TBI.
RESEARCH JOURNAL

125. Methods:
A large cohort of community-based patients with TBI, recruited from a TBI rehabilitation program,
completed measures of subjective fatigue and sleep disturbances, as well as attentional measures.
A subgroup of participants completed polysomnography and assessment of dim light melatonin
onset.
Results:
➤ Fatigue and sleep disturbance are common. Both are associated with anxiety, depression, and
pain. However, fatigue is also associated with slowed information processing and the need for
increased effort in performing tasks. Sleep disturbances contribute to fatigue. Objective sleep
studies show reduced sleep efficiency, increased sleep onset latency, and increased time
awake after sleep onset. Depression and pain exacerbate but cannot entirely account for these
problems. There is increased slow-wave sleep. Individuals with TBI show lower levels of evening
melatonin production, associated with less rapid-eye movement sleep.
Conclusions:
➤ These findings suggest potential treatments including cognitive behavior therapy supporting
lifestyle modifications, pharmacologic treatments with modafinil and melatonin, and light
therapy to enhance alertness, vigilance, and mood. Controlled trials of these interventions are
needed.
RESEARCH JOURNAL

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