FRANCIS ANTHONY B.

LOSLOSO
ASSIGNMENT #3

Traumatic brain injury is a major cause of death and disability in adults. It is a complex phenomenon
with results ranging from no detectable effect to persistent vegetative state. Trauma can result in
hemorrhage, contusion or laceration of the brain and damage at the cellular level. In addition to the
primary insult, the brain injury may be compounded by cerebral edema, hyperemia or hydrocephalus.

The brain is susceptible to various types of injury:

✓ Closed head injury/ non-penetrating injury- rapid back and forth movement of the brain
causing bruising and tearing of brain tissues and vessels but the skull is intact
✓ Open head injury/ penetrating injury- break in skull
✓ Acceleration injury- moving objects hitting a stationary head
✓ Deceleration injury- head is in motion and strikes a stationary surface

1. Three major categories of craniocerebral injury

*Note: Some resources states that the three major categories are focal brain injury, diffuse brain
injury and skull fracture, some are classified according to severity such as mild moderate severe)

a. Skull fractures
i. Diastatic- fractures that cross sutures
ii. Displaced skull fracture- bone is displaced into the cranial cavity by a distance
greater than the thickness of the bone. The thickness of the cranial bones varies,
their resistance to fracture differs greatly.
iii. Multiple points of impact or repeated blows to the head, the fracture lines of
subsequent injuries do not extend across fracture lines of prior injury
iv. Falls related injury incidence
✓ Conscious patient- occipital impact
✓ Due to syncope follows loss of consciousness- frontal impact
✓ Basal skull fractures- occiput or sides of the head rather than vertex, difficult
to detect
✓ Symptoms related to cranial nerves, cervicomedullary region-orbital or
mastoid hematomas distant from point of impact; CSF discharge from nose
or ear and infections may follow

b. Parenchymal injuries
i. Concussion (Mild brain injury)- brought by closed head injury characterized by
sudden onset and transient neurologic dysfunction, including loss of consciousness,
respiratory arrest, loss of reflexes.
✓ Neurologic recovery is complete, but amnesia for the event persists.
✓ It is reversible and unassociated with permanent structural damage
✓ Increasing evidence of biochemical abnormalities do occur such as depletion
of mitochondrial adenosine triphosphate as well as possibly ultrastuctural
changes
 ii. Direct Parenchymal Injury
✓ Contusion (Bruising of the brain possibly accompanied by hemorrhage)-
transmission of kinetic energy to the brain and bruising analogous to what is
seen in soft tissues
• Most often occur on the surface of the brain at sites where the brain
contacts rough bony surfaces, such as tips of the temporal lobes,
inferior frontal surfaces and the occipital poles.
• Severe contusions can result in diffuse axonal injury.
• Symptoms depends on the area of the brain involved
i. Brain stem- affects LOC
ii. Respirations, pupil reaction, eye movement, motor response
to stimuli may also be affected
iii. ANS may be affected by edema or hypothalamic injury
causing rapid HR and RR, fever and diaphoresis
• A blow to the surface of the brain, transmitted through the skull
leads to rapid tissue displacement, disruption of vascular channels
and subsequent hemorrhage, tissue injury and edema
• The pattern of the lesions reflects the distribution of the applied
force: the crests of gyri are most susceptible, whereas sulci are
relatively uninvolved
• Lesions occur where the direct impact of trauma can reach the brain
surface, and thus tend to spare the contents
• Contusions, when seen on cross-section, often have a wedge-shaped
appearance, with the broad base spanning the surface and centered
on the point of impact
• Coup injury- suffers a blow with a discrete point of impact may
develop only minimal injury underlying the point of contact
i. Caused by direct impact
• Contrecoup injury- brain opposite to it may show extensive damage
i. Impact of brain with the opposite inner surface of the skull
fowling sudden deceleration
• Coup and contrecoup are result of sudden deceleration of the head
and are not seen when the head is immobile
✓ Laceration- penetration of an object and tearing of tissue
iii. White matter injury
✓ Involves white matter
✓ Often deep within the brain
✓ Includes axonal retraction balls indicative of diffuse axonal injury or focal
hemorrhagic lesions
✓ Well demonstrated by silver staining, being found most commonly in the
corpus callosum and the dorsal lateral brain stem and less often in the
pontine tegmentum
c. Traumatic vascular injuries- frequent component of CNS trauma and result from direct
trauma and disruption of the vessel wall, leading to hemorrhage.
i. Epidural hematoma
✓ Epidural space is a potential space- the dura is closely applied to the internal
surface of the skull and is fuse with the periosteum.
✓ Vessels that course within the dura, most importantly the middle meningeal
artery are vulnerable to injury, particularly with skull fracture
✓ Trauma to the skull, especially in the region of the temporal bone can lead
to laceration of this artery if the fracture lines cross the course of the vessel
✓ In children-skull is deformable, a temporary displacement of the skull bones
leading to laceration of a vessel can occur in the absence of skull fracture
✓ Once vessel has been torn, accumulation of blood, under arterial pressure,
can lead to dissection of the dura from the inner surface of the skull
✓ Expanding mass will have a smooth inner contour that compresses the
cortical surface
✓ Patients are often lucid for several hours between the moment of trauma
and the development of neurologic signs
✓ It may expand rapidly and is a neurosurgical emergency requiring prompt
drainage
ii. Subdural hematoma
✓ Maybe acute or chronic
✓ Space beneath the inner surface of the dura mater and the arachnoid layer
of the leptomeninges is a potential space
✓ Vessels are particularly susceptible to tearing along their course through the
subdural space and are the source of bleeding in most cases of subdural
hematoma
✓ Most commonly accepted mechanism of damage postulates that the brain
floating freely within the skull in its bath of CSF, can move within the skull,
but the venous sinuses are fixed
✓ The displacement of the brain that occurs in trauma can tear the veins at
the point where they penetrate the dura
✓ Brain atrophy in elderly, bridging veins are stretched out and the brain has
additional space for movement, hence the increased rate of subdural
hematoma even after relatively minor head trauma
✓ Often manifest within the first 45 hours after injury
✓ Most common over the lateral aspects of the cerebral hemispheres and are
bilateral in about 10% of cases
✓ Neurologic signs commonly observed are attributable to the pressure
exerted on the adjacent brain
✓ Focal signs, but often with manifestations are nonlocalizing (headache,
confusion)
✓ Overtime, slowly progressive neurologic deterioration but rarely acute
decompensation
iii. Subarachnoid hemorrhage and Traumatic intraparenchymal hematoma
 ✓ Occur from a variety of nontraumatic conditions
✓ Most causes of traumatic SAH commonly associated with parenchymal
trauma
✓ Contusion of superficial cerebral tissue or, less frequently, cerebellar cortex
is associated with disruption of small vessels within both the brain
parenchyma and the overlying leptomeninges
✓ Direct vascular injury, such as laceration of a normal vessel or rupture of a
pre-existing aneurysm or malformation can lead to the accumulation of
blood in the subarachnoid space in the absence of parenchymal injury

2. 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 result in
axonal swelling and disconnection. Clinically, with severe injury, the patient has no lucid intervals
and experiences immediate coma, decorticate and decerebrate posturing and global cerebral
edema.
a. It is a brain injury in which extensive lesions in white matter tracts occur over a widespread
area. It is one of the most common and devastating types of traumatic brain injury, and is a
major cause of unconsciousness and persistent vegetative state after severe head trauma.
b. Mechanism:
It is the result of traumatic shearing forces that occur when the head is rapidly accelerated or
decelerated, as may occur in car accidents, falls and assaults. Vehicle accidents are the most frequent
cause of DAI. It can also occur as the result of child abuse such as in shaken baby syndrome.
Immediate disconnection of axons could be observed in severe brain injury but the major damage
of DAI is delayed secondary axon disconnections slowly developed over an extended time course.
Tracts of axons, which appear white due to myelination are referred tot as white matter. Lesions in
both grey and white matters are found in postmortem brains in CT and MRI exams.
Besides mechanical breaking o the axonal cytoskeleton, DAI pathology also includes secondary
physiological changes such as interrupted axonal transport, progressive swellings and degeneration.
Recent studies have linked these changes to twisting and misalignment of broken axon microtubules
as well as tau and APP deposition

3. Mr. Ga’s CT scan may be positive due to his signs of unresponsiveness accompanied by irregular
breathing and epistaxis. The CT scan may show multiple results depending on the affected part of
the brain. Identifying hypodense parts through CT may indicate that there is bleeding or air inside
the brain therefore compressing the surrounding brain tissues and may signify different
manifestations.

4. Prior transporting the patient, the EMT nurse should be able to establish baseline vital signs and
LOC, rapid neuro assessment including GCS score and pupillary response, C-spine stabilization
must be done and follow ABC steps.

5. Mr. Ga’s ABG is interpreted as acute/ uncompensated respiratory acidosis

 He might be suffering from brain stem damage probably herniation compromising his
breathing as manifested as irregular breathing in depthness and rate. The pons and
medulla are responsible for respiration.

6. FiO2 at 0.35%
a. Oxygen in the body is vital especially the patients respiratory is impaired. The level of
oxygen needed is equivalent to 4 liters/ min. It is enough to stimulate the body from
hypoxic drive despite the patients CO2 level is high. It will also prevent oxygen toxicity that
is harmful.
b. However, Mechanical hyperventilation is recommended if with increased ICP. It is effective
in lowering ICP because it causes vasoconstriction. It allows less blood into the cranium
thereby lowering ICP.
c. Aggressive hyperventilation within the first 24 hours after injury may induce ischemia in
the already compromised brain. Hyperventilation is reserved for increased ICP that does
not respond to other treatments

7. Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction

(cerebral blood vessels) thus lowering cerebral blood flow, cerebral blood volume and ICP. This
effect is mediated by pH changes in the extracellular fluid which cause cerebral vasoconstriction or
vasodilation depending on the pH.

8. Complications in head injury with pulmonary problem

Possible complication related to pulmonary problem is pneumonia due to immobility and pooling
of secretions inside the lungs further developing infections and will contribute in compromising
patient’s respiratory status

9. IV solutions for Mr. Ga

a. Crystalloid solution- mixture of NaCl and other physiologically active solutes
i. Physiologic saline and Hartmann’s solution- commonly used crystalloids with
identical volume expanding effects. They distribute throughout extracellular space.
Aggravation of cerebral edema is minimal if hypo-osmolality is avoided
b. Solutions of 5% glucose with saline are essentially water rendered isotonic to prevent
hemolysis, and at most infusion rates, insufficient glucose is infused to raise glucose levels
in blood and fluid in distributed throughout total body water. Thus, for every liter of
solution infused, 2/3 will enter intracellular space and 1/3 will be in the extracellular space.
Glucose infusion promotes anaerobic glycolysis and lactic acidosis in the setting of cerebral
ischemia and infusion of such fluids should be avoided in vulnerable patients.
c. Hypertonic saline- reduce raised ICP. Rapid infusion of small volume of hypertonic saline
leads to an osmotic gradient that draws water into the intravascular compartment with
osmosis of parenchymal fluid.
d. Colloidal solutions- effective in restoring blood volume by withdrawing extracellular fluid
into the intravascular compartment by virtue of colloid osmotic pressure. High molecular
weight compounds like albumin and urea bridged gelatin are retained in the intravascular
compartment and produce an oncotic gradient that tends to retain water in the capillaries.
10. Mr. Ga exhibiting decorticate posturing and GCS of 5
a. Decortication (flexion, adduction and internal rotation of upper extremities, lower
extremities are extended)
i. Involvement above the midbrain
b. Decerebration (extension, adduction, and internal rotation of the arms and extension of
lower extremities)
i. Involvement of the brainstem
ii. Indicates poor prognosis
iii. Risk for cardiopulmonary arrest
c. Glasgow coma scale of 5 is low signifying that the patient is experiencing severe brain
injury
i. 3-8 severe brain injury
ii. 9-12 moderate brain injury
iii. 13-15 minor brain injury

11. Cushing’s triad

a. Increase in systolic blood pressure- initial response to rising ICP.
b. Widening pulse pressure
c. Decreased heart rate
*As ICP continues to increase, the patient’s heart rate will increase, breathing will became shallow,
periods of apnea will occur and blood pressure begin to fall
12. Drugs usually given to neuro patients
a. Lasix- it is a loop diuretic, it acts on the loop of Henle and helps in reducing cerebral edema
by increasing urine output
b. Mannitol- osmotic diuretic that reduces cerebral edema by increasing urine output. It
utilizes osmosis to pull fluid into the intravascular space and eliminate it via the renal
system. Serum osmolarity and electrolytes must be carefully monitored when mannitol is
being administered
 c. Nursing implications would be to monitor patients input and output accurately, ensuring
that mannitol will be given fast drip or bolus because it crystalizes. Monitoring electrolyte
balances and glucose is important.

13. Other drugs could be given to assist in the action of Lasix and Mannitol
a. Dexamethasone- corticosteroid, anti-inflammatory effect and reduces cerebral edema.
Only steroid that can pass the blood-brain-barrier
b. Anticonvulsants- to prevent seizures
c. Antacids- to prevent GI irritation caused by dexamethasone
d. Histamine receptor agonist- to prevent stress ulcer (Cushing’s ulcer)
e. Anticoagulants- to prevent thromboembolism
f. Anti-hypertensive

14. Role of barbiturate therapy in head-injury patients

a. High-dose barbiturate therapy may be used to induce a therapeutic coma, which reduces
the metabolic needs of the brain during the acute phase following injury.
b. Patients are completely dependent for all their needs and care. They will be mechanically
ventilated and cared for in an ICU setting.
c. Vasopressors may be required to maintain blood pressure and the patient’s temperature
should be kept as normal as possible

15. Orogastric tube for GIT decompression

a. Traumatic brain injured patients may also have basilar skull fracture (periobital ecchymosis
or Battle’s sign may not manifest itself for a few hours) and there may be associated facial
fractures. Therefore, an orogastric tube instead of nasogastric tube should be inserted.
Gastric decompression is important to prevent aspiration and to prevent gastric inflation if
associated with respiratory arrest, but the nasal route should be avoided initially until all
other injuries are ruled out

16. ICP= 18mmHg, BP- 80/50

Interpretation: Mr. Ga has increased ICP and exhibiting hypotension probably due to use of
diuretics.
a. Intra-Cranial Pressure- pressure exerted within the cranial cavity by its components
b. Blood, Brain, Cerebrospinal Fluid
c. Normal ICP= 0-15mmHg
d. Pressure fluctuates with normal physiologic changes such as arterial pulsations, changes in
position and increases in intrathoracic pressure
e. Common cause:
i. Brain trauma
ii. Intracranial hemorrhage
iii. Brain tumors
f. If an increase in one component is not accompanied by a decrease in one or both of the
other components, the result is increase ICP
g. Consequences depend on the degree of elevation and the speed with which ICP increases
h. Signs and symptoms:
i. Restlessness- initial sign of ICP
ii. Headache- traction on pain- sensitive brain structures and on cranial nerves
iii. Nausea/ vomiting- pressure at the medulla oblongata. May exhibit projective
vomiting
iv. Irritability
v. Decreased LOC- due to impaired cerebral cortex function, affectation of ascending
reticular activating system
vi. Hyperventilation if not yet intubated causing body to compensate
(vasoconstriction)
vii. Diplopia (double vision)- pressure on the CN VI which controls the lateral rectus
muscle of the eye. CN VI- longest CN, prone to compression
viii. Anisucuria (unequal pupil)- due to CN III compression. Ipsilateral pupil dilation
ix. Pinpoint pupils indicate pons involvement
x. Papilledema- compression of optic nerve
xi. Diminished reactivity and dilation of the pupil- compressed oculomotor nerve on
the side of the impairment
✓ Increased in compression- pupils stops reacting to light
✓ Continuous compression- pupils become fixed and dilated (brainstem
herniation), leading to cardiac arrest
xii. Cushing’s triad- stimulation of Cushing reflex in response to cerebral hypoxia
✓ Blood pressure
• Elevated systolic pressure- increased force of cardiac contractility,
body attempts to increase cerebral tissue perfusion and oxygenation
• Diastolic pressure remains normal or decreased- longer time
required or the heart to relax
• Widening pulse pressure- more than 40mmHg
✓ Bradycardia
✓ Bradypnea- involvement of medulla oblongata and pons
xiii. Changes in body temperature- involvement of hypothalamus
xiv. Doll’s Eye sign- dysconjugate movement of the eyes as the head is moved to one
side
xv. Decortication and decerebration
xvi. Agnosia
xvii. Seizure
xviii. Expressive aphasia, receptive aphasia, alexia
xix. Bowel and bladder function (retention and incontinence)

i. Cerebral Perfusion Pressure- blood flow to the brain

i. Blood pressure and intracranial pressure affect the CPP
ii. Monitoring and managing CPP is a key component of the management of TBI. It is
easily measured, can be monitored continuously and maintenance of CPP sufficient
to sustain adequate cerebral blood flow.
 iii. It is the pressure driving blood through the cerebrovascular bed, and therefore the
difference between the inflow and outflow pressures.
iv. CPP is determined in clinical practice as the difference between MAP and mean ICP
v. Mean arterial pressure (MAP)- commonly measured at the level of the right atrium
using mid-axillary line at the 4th ICS as the zero-reference point for the arterial
transducer. This provides the most valid determination of arterial blood pressure
and is equivalent to the pressure measured by standard sphygmomanometer
techniques.
vi. In supine position, the head resting in a neutral position, the tragus has roughly the
same elevation as the RA and when calculating CPP, it is reasonable to assume that
the MAP at the level of the heart and brain is identical. However, when the head is
elevated above the heart hydrostatic effects mean that cerebral arterial blood
pressure, will be reduced by a magnitude dependent on the angle of elevation and
distance between RA and brain reference points.
vii. Computation and interpretation (MAP-ICP= CPP)
✓ Low CPP <60mmHg
• Risk for further neurological injury from cerebral hypoperfusion
• Increase MAP (vasopressors, fluid bolus) or decrease ICP (elevate
head of bed, mannitol, CSF drainage)
✓ Normal CPP 60-70mmHg
• Adequate cerebral perfusion
✓ High CPP >70mmHg
• Unlikely to benefit from CPP this high and may be at increased risk
for hypoxemic respiratory failure and ARDS, which can contribute to
cerebral ischemia and prolonged mechanical ventilation
viii. Computation
Systolic BP- 80
MAP= SBP + 2(DBP) / 3
80 + 2(50) / 3
80 +100 / 3
180/3= 60mmHg
MAP- ICP= CPP
60-18 = 42mmHg

17. Nursing Management for Mr. Ga

a. Positioning: Semi-fowlers- promote drainage of CSF from subarachnoid space. Promote
maximum lung expansion. Do not elevate to 90 degrees, may cause brain herniation. Limit
elevation from 15-45 degrees
b. Oxygenation: Mechanical ventilation helps promote acid-base balance. Acidosis and
alkalosis may increase ICP
c. Monitor pupil responses, level of consciousness and thorough neurologic assessment, NVS
q1
d. Reorientation
e. Fall precaution due to altered level of consciousness
 f. Avoid Valsalva maneuver, over suctioning, rectal exam, coughing, sneezing, bending,
nausea, vomiting
g. Decrease stimuli
h. Control hypertension
i. Administer diuretics such as Mannitol and Lasix- monitor BP

18. Potential complications

a. Brain herniation- due to uncontrolled increased ICP. Displacement of brain tissue out of its
normal anatomical location. This displacement places pressure on other vital organs
commonly the brainstem resulting to brain death.
b. Diabetes insipidus- edema or direct injury affects the posterior portion of the pituitary
gland or hypothalamus. Inadequate release of ADH results in polyuria and if the patient is
awake, polydipsia. Ensure fluid replacement and IV vasopressin to maintain fluid and
electrolyte balance
c. Acute hydrocephalus- cerebral edema can interfere with CSF circulation. Manage with
ventriculoperitoneal shunt if necessary.
d. Labile vital signs- direct trauma or pressure on brainstem can cause fluctuations in blood
pressure, heart rate and respiratory rate
e. Posttraumatic syndrome
f. Cognitive and personality changes- long term complication. May have short term memory
impairment.

19. In craniocerebral injuries, particularly trauma, little can be done, for it is finished before the
physician or others arrive on the scene. Assessment of the full extent of the immediate cerebral
injury, evaluation of factors conducive to complications and further lesions, and the institution of
measures to avoid such additional problems.

In some extent, with good health care delivery system, well-trained EMT that will respond to Mr.
Ga’s MVA, well-coordinated transport and dedicated and proper health care management, Mr.
Ga’s may be hopeful. Nothing is impossible, everything can be reversed depending on the degree
of severity of Mr. Ga’s condition. With unresponsiveness and irregular breathing alone, we cannot
really determine the extent of damage done to the brain, we just know that there is a breathing
problem probably affecting the brain stem.

This case study is very broad in terms of alterations in perception. In order for one to appreciate
the beauty of this case is that one must master anatomy and physiology before proceeding to
pathophysiology. Literally, every response of the patient depends on where the trauma in the brain
happens. Every lobe has different function and each of which has different set of manifestations. I find
this very helpful and it really challenged me a lot.