Traumatic Brain Injury

• Traumatic brain injury (TBI), also known

as intracranial injury, occurs when an external
force traumatically injures the brain.
 Definition
• Traumatic brain injury (TBI) is a
nondegenerative, noncongenital insult to the
brain from an external mechanical force,
possibly leading to permanent or temporary
impairment of cognitive, physical, and
psychosocial functions, with an associated
diminished or altered state of consciousness.
 
• Head injury usually refers to TBI, but is a
broader category because it can involve
damage to structures other than the brain,
such as the scalp and skull.
 Causes
• Falls (47.2%)
• Being struck by or against objects (15.4%)
• Motor vehicle crashes (13.7%)
• The US Center for Disease Control (CDC)
states that children are more at risk for
traumatic brain injury due to regular physical
play and participation in youth sports. Babies
and toddlers are susceptible due to
underdeveloped skulls and balance abilities.
The elderly (especially those in nursing
homes) are at risk due to age-diminished
strength, balance, and bone frailty.
 Causes

• Primary causes of TBI include falls, blunt trauma, and motor vehicle accidents:
• The Centers for Disease Control and Prevention (CDC) and Brain Injury
Association of America (BIA-USA) state that
• children 0-4 years of age and 15-19 years of age are at the greatest risk for TBI.
• Males and females 10-19 years of age experience TBI during sports/recreation
activities, such as basketball, cheerleading, football, ice hockey, and soccer.
• Motor vehicle accidents are the leading cause of brain injury and death for
individuals age 15-20 years.
• Children and older adults are more susceptible to TBIs from falls than other
age groups.
Pathophysiology
• Immediately following a brain injury, two things occur:
 Brain tissue reacts to the trauma from the injury with a
series of biochemical and other physiological responses.
Substances that once were housed safely within these cells
now flood the brain, further damaging and destroying brain
cells in what is called secondary cell death.

 Depending on the severity of brain injury, effects may

include temporary loss of consciousness or coma, respiratory
(breathing) problems, and/or damaged motor functions.
Classification of brain INJURY
• Severity of TBI Based on the Duration of
LOC Severity of TBI
• Mild
• Mental status change or LOC < 30 min
• Moderate
• Mental status change or LOC 30 min to 6 h
• Severe
• Mental status change or LOC > 6 h
• Closed TBI: This is the most common type of brain
injury. This is defined by a non-penetrating blow to
the head and is most commonly experienced as a
concussion. Nearly 75 percent of all TBIs involve
some form of concussion.
• Open TBI:  Typically a more severe injury and applies
to any case in which the skull is broken or
penetrated and the brain is physically damaged by
the object or by broken skull fragments being push
into the brain.
• Diffuse vs. Localized Damage
• Localized Damage
Localized damage occurs in a specific location. Localized damage is
commonly associated with an injury in which the head strikes or is
struck by an object. This usually occurs following an open/penetrating
traumatic brain injury.
• Diffuse Damage
Diffuse damage occurs over a widespread area. Diffuse damage is
commonly associated with acceleration/deceleration injuries, in which
the head does not necessarily contact anything, but brain tissue is
damaged. This often occurs in a closed traumatic brain injury.
• Many traumatic brain injuries cause both localized and diffuse
damage.
• Diffuse Axonal Injury

A diffuse axonal injury can be caused by shaking

or strong rotation of the head, as with shaken
baby syndrome, or by rotational forces, such
as with a car accident.
• Concussion/Mild Traumatic Brain Injury (mTBI)
• A concussion can be caused by direct blows to
the head, gunshot wounds, violent shaking of
the head, or force from a whiplash-type injury.
Both closed and open head injuries can
produce a concussion. A concussion is the
most common type of traumatic brain injury.
• Contusion
A contusion is a bruise (bleeding) on the brain
caused by a force (blow or jolt) to the head.
Coup-Contrecoup Injury
• Coup-contrecoup injury describes contusions
that are both at the site of the impact and on
the complete opposite side of the brain. This
occurs when the force impacting the head is
not only great enough to cause a contusion at
the site of impact, but is also able to move the
brain and cause it to slam into the opposite
side of the skull.
Second Impact Syndrome
• Second impact syndrome, also termed "recurrent
traumatic brain injury," can occur when a person
sustains a second traumatic brain injury before the
symptoms of the first traumatic brain injury have
healed. The second injury may occur from days to
weeks following the first. Loss of consciousness is
not required. The second impact is more likely to
cause brain swelling and widespread damage.
• Penetrating Injury
Penetrating injury to the brain occurs from the
impact of a bullet, knife, or other sharp object
that forces hair, skin, bone, and fragments
from the object into the brain.
• Abusive Head Trauma (Shaken Baby Syndrome)
Abusive head trauma, also known as shaken
baby syndrome, is a violent criminal act that
causes traumatic brain injury. Abusive head
trauma occurs when the perpetrator
aggressively shakes a baby or young child. The
forceful whiplash-like motion causes the brain
to be injured.
 Types od neurologic Damage
Primary Damage

Damage that occurs at the time of actual impact.

There are many types of primary damage that may occur. These include:
Coup-Contrecoup Injury- damage to the brain on both sides: the side that received the initial impact (coup) or blow
and the side opposite the initial impact (countrecoup). This occurs when the force of the initial blow is great enough
to cause brain damage at the site of initial impact between the skull and brain and is also great enough to cause the
brain to move in the opposite direction and hit the opposite side of the skull, causing damage at that site.
Skull Fracture- breaking of skull bone
Contusion/Bruise- discoloration and/or swelling at the location of actual impact or at the point or points where the
force of the blow has driven the brain against the skull’s bony ridges
Hematoma/Blood Clot- swelling or mass of blood between the skull and the brain or inside the brain itself
Laceration- tearing of brain tissue and/or blood vessels, caused by forceful rotation of the brain across the skull’s bony
ridges
Nerve Damage (Diffuse Axonal Injury)- shearing or tearing of white matter in connecting nerve fibers in the brain; can
cause unconsciousness and/or coma
• Secondary Damage
Damage that occurs over time after the actual brain
injury; may include infection, hypoxia (oxygen
deprivation), edema (brain swelling), elevated
intracranial pressure, infarction (death of brain
tissue which results in loss of blood supply to that
region of the brain), and hematoma (focal area of
bleeding in the skull due to tearing of blood
vessels). Many traumatic brain injuries result in
multiple types of primary and secondary damage.
 Complications
• Posttraumatic seizures: Frequently occur after moderate or severe TBI
• Hydrocephalus
• Deep vein thrombosis: Incidence as high as 54% [6]
• Heterotopic ossification: Incidence of 11-76%, with a 10-20%
incidence of clinically significant heterotopic ossification [7]
• Spasticity
• Gastrointestinal and genitourinary complications: Among the most
common sequelae in patients with TBI
• Gait abnormalities
• Agitation: Common after TBI
• Chronic traumatic encephalopathy (CTE)
• Insomnia
• Cognitive decline
• Posttraumatic headache: Tension-type headaches are the most
common form, but exacerbations of migraine-like headaches
are also frequent
• Posttraumatic depression: Depression after TBI is further
associated with cognitive decline
• anxiety disorders
• substance abuse
• dysregulation of emotional expression
• aggressive outbursts
Prehospital Management
 Diagnosis
• GCS
• MRI & CT SCAN
 Management of Increased ICP
• Sedation and Analgesia :
• Propofol is usually the drug of choice for sedation
because of its rapid onset and short duration. 
• Midazolam is the preferred benzodiazepine because
of its shorter half-life compared to lorazepam, easier
titration, and status as the most studied drug in TBI.
*****Since midazolam is not that effective in ICP control

alone or in combination with propofol, it is used in

patients who cannot receive propofol due to adverse
effects14
• Opioid therapy:
• Morphine is widely used as a continuous infusion or intermittent bolus.
• Fentanyl and remifentanil are also used because of their shorter duration of action as
a continuous infusion.
***These medications are recommended because they provide analgesia, mild
sedation, and depression of airway reflexes, which is necessary for intubated and
mechanically ventilated patients.
• Miscellaneous agents
• loop diuretics can be used as second-line therapy for fluid overload patients to
decrease ICP.
• Neuromuscular blockers (NMBs) have also been used concomitantly for patients who
are receiving maximum tolerated doses of propofol or who are refractory to all other
agents for ICP control.  Although NMBs may not have any direct effect on lowering of
ICP, they may be beneficial for facilitating mechanical ventilation, minimizing muscle
activity and spasms, and improving respiratory compliance.
• Hyperosmolar Therapy: Mannitol is very
effective in lowering ICP in severe TBI. It works
as an osmotic diuretic that creates an osmotic
gradient, thereby increasing the serum
osmolarity up to 310 to 320 mOSM/kg H2O in
order to pull extracellular fluid from the brain.
• Hypertonic saline solution (HSS) 3% to 23.4% is an
effective alternative to mannitol, and in some
studies has been found to be superior. This
alternative therapy causes osmotic dehydration and
viscosity-related cerebral vasoconstriction. The
beneficial effects of HSS in TBI include expansion of
intravascular volume, extraction of water from the
intracellular space, decrease in the ICP, controlled
cerebral edema, and an increase in cardiac
contractility.
• Temperature Modulation: Moderate
hypothermia may be used in refractory,
uncontrolled ICP. Moderate systemic
hypothermia at 32°C to 34°C has shown
evidence in reducing cerebral metabolism and
cerebral blood volume, decreasing ICP, and
increasing CPP.
• Barbiturate Coma: Barbiturates have been proven
effective therapies for refractory or second-line
intracranial hypertension. They reduce cerebral
metabolism and cerebral blood flow and lower
ICP. Pentobarbital is recommended for the
induction of barbiturate coma. It is recommended
in hemodynamically stable, severe TBI patients
who are refractory to maximum medical and
surgical ICP-lowering therapy.
 Seizure Management
• According to the American Academy of Neurology, among all patients with head trauma who seek medical
attention, about 2% develop posttraumatic seizures, although the number differs extensively depending
primarily on injury severity. About 12% of patients with severe TBI develop posttraumatic seizures, and the rate
may be greater than 50% for those with penetrating missile injuries. 9
• Posttraumatic seizures can be classified in two ways—as early or late onset.
 Early-onset seizures occur within 7 days of injury,
 Late-onset seizures occur 7 days after injury.

Prophylactic therapy with antiepileptic drugs (AEDs) is not recommended for preventing late posttraumatic
seizures. However, it is recommended for prophylactic therapy to prevent early posttraumatic seizure in TBI
patients who are at high risk for seizures. High-risk patients are defined as having the following: GCS score <10,
cortical contusion, depressed skull fracture, subdural hematoma, epidural hematoma, intracerebral hematoma,
penetrating TBI, and seizures within 24 hours of injury. Phenytoin is the drug of choice for the prophylaxis of
early posttraumatic seizures. A loading dose of 15 to 20 mg/kg administered IV over 30 minutes followed by
100 mg IV every 8 hours, titrated to recommended plasma level for 7 days.  9,13
• Alternatively, levetiracetam has been studied and showed benefit, and is potentially as efficacious as phenytoin
at doses of 500 to 1,000 mg twice daily for 7 days.

• Both valproate and phenobarbital have been studied and have demonstrated little benefit in posttraumatic
seizures in high-risk TBI patients. Patients receiving AED prophylaxis should be monitored for potential side
effects. Preventive therapy beyond the first 7 days of injury is not recommended. 17-19
 Surgical Therapy
• Decompressive craniectomy or
hemicraniectomy is an option for patients with
acute severe TBI who are at risk for developing
severe brain edema and intractable
intracranial hypertension in cases where
medical management fails.
 Non Pharmalogical Therapy
• Elevating the head of the bed at a 30-degree
angle in hemodynamically stable patients and
CSF drainage in patients with ventriculostomy
can be recommended. Both methods have
been shown to decrease ICP.
 
 Prognosis
• Mortality rates after brain injury are highest in
people with a severe TBI.
• In the first year after a TBI, people who survive
are more likely to die from seizures, septicemia,
pneumonia, digestive conditions, and all
external causes of injury than are other people
of similar age, sex, and race. 
• However, the mortality rate after severe TBI has
decreased since the late 20th century
• Assignment (Hand Written)
Write the three prioritised Nusing Daignosis of
patient with TBI With Nursing intervention
Marks : 25
Date of Submission : 1/4/2020