CARUNUNGAN, Karen Crystal J.

BSRT-2
Submitted on: 10/05/20
Traumatic Brain Injury
SCORE:40/50
A Case Report CONTENT: 20/25 ORGANIZATION: 12/15 MECHANICS: 8/10
COMMENTS: The case lacks further details especially the diagnostic
Part I. procedure and the plan for the AV malformation seen on imaging.
Also, imaging could have been included. While the discussion is
good, it failed to discuss the main presentation of the patient, which
A. PATIENT INFORMATION is seizure, given that the AV malformation does not produce any
• NAME : Unknown compressive effect as per imaging. The facts in the discussion were
not used to analyze the case.
• AGE: 28 years old
• GENDER: Male
• ETHNICITY: White/Caucasian

CHIEF COMPLAINT/PRIMARY CONCERN

• Unconscious due to Motor vehicle Accident/ Trauma

HISTORY OF PRESENT ILLNESS

• On October 30, 2014, a 28- year old, white male was found by bystanders in prone position,
unconscious after he had lost control of his motorcycle and went off road.

RELEVANT PAST INTERVENTIONS AND OUTCOMES

• Patient was unconscious and was brought to an Emergency department by an ambulance and
was intubated at Level 1 Trauma.

B. CLINICAL FINDINGS
• initial GCS score of 3T, 4 mm bilaterally fixed pupils, negative corneal response, right parietal
cephalohematoma, and cerebral spinal fluid otorrhea on the right. (since patient is intubated,
verbal assessment is not possible thus score of “T”)

• Patient is bradycardic with the lowest recorded data as 28 bpm.

• Patient’s blood pressure increased from an initial record of 172/118 mmHg to 221/105 mmHG
within 30 minutes interval

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20
C. DIAGNOSTIC ASSESSMENT

• CT scan of he head

a. subarrachnoidal hemorrhage with left frontal and temporal subdural

hemorrhage.

b. Effaced suprasellar cistern and left temporal subdural hemorrhage

c. Effacement of the suprasellar cistern, and effacement of the 3 rd and 4th

ventricles.

d. left fronto-temporal and parietal hematoma with mass effect and cerebral
edema causing 5.38 mm left to right midline shift, a frontal skull bas
fracture, and a complex, non-displaced comminuted fracture of the right
temporal bone.

• chest x-ray reveals worsening in his bibasilar opacities

• Respiratory Culture:

◦ methicillin-sensitive staphylococcus aureus (>10 000 cfu/ml)

◦ pseudomonas aeuginosa (>10 000 cfu/ml)

• Fecalysis: Positive for clostridium difficile toxin B (14th dat inpatient)

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20
• Bronchoscopy using saline lavage was done due to copious amounts of think, tan endotracheal
secretions

D. THERAPEUTICS, PATIENT OUTCOME AND FOLLOW-UP

• Initial Therapeutics (ED)

◦ Administration of fluid – to provide fluids to the body and for the administration of medication
since patient is unconscious and intubated and medications given orally is impossible.

◦ Nicardipine drip/infusion – to treat hypertension

◦ Atropine push – to manage bradycardia. It increases the heart rate and improves cardiac
contraction.

◦ Intubation/Endotracheal Intubation done – to open airway.

◦ 30 grams of IV Mannitol – for reduction of ICP and reduction of brain mass/swelling which is
cause by the trauma.

◦ 23%NaCl – to decreased ICP

• Surgical Therapy:

◦ Left-sided decompression Craniectomy – a neurosurgical process of opening a part of the

skull, in this situation the left side, to give room for the swelling brain to expand without
being squeezed. The part of the skull being removed will be p;laced under the skin of the
abdominal area for it to have ample blood supply.

◦ Extra Ventricula Drain placement – to treat or relieve increased ICP due to obstruction of the
normal flow of CSF.

◦ Outcome: Patient’s condition improves

▪ His GCS was 5T, with bilaterally active pupils, and positive corneal reflex in the left eye.

▪ ICP using the EVD of 14 mmHg.

▪ Repeat CT scan reveals:

a. improved midline shift and evolving bilateral traumatic subarachnoid

hemorrhage

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20

b. the ventriculostomy cathether tip can be seen properly placed in its correct
position in the frontal horn of the right lateral ventricle

• Medication:

◦ IV Vancomysin – to treat infection, it showsa that the patient acquire a lung infection as
shown on the opcaity of his chest xray

◦ IV Levofloxacin and IV Cefepime – a drug combunation to treat MRSA pneumonia by

preventing the bacteria to form a protective covering.

◦ IV Zosyn – a penicillin-class antibacterail (1st class) to treat patient’s pneumonia but later on
was ordered back to vancomysin since the causative agent of the patient’s pneumonia is
piperacillin/tazobactam-resistant pseudomonas pneumoniae. Which is penicillin resistant.

◦ Metronidazole – to treat loosse watery stool cause by c. difficile toxin b, an infection caused
by the patient’s medication history of different antibiotics.

• Ventilator:

◦ increase in FiO2 from 50% to 80% and PEEP to supply higher oxygenation level since there
is an impairment of flow.

◦ changing ventilator settings to APRV mode. - since patient’s oxygenation is improving. It is

a way to prepare the patient for weaning.

• Therapy:

◦ Speech therapy to treat his speech disorder due to previous head and brain trauma. Also,
aides in the helping the patient swallow properly.

• Follow-up

◦ after three months

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20
▪ patient has improved. Tracheostomy and and gastrostomy was removed and
neurologically stable.

◦ After 11 months

▪ patient is still stable with an improvement with is speech.

References:

Zach, V.(2016). Severe traumatic barin injury: A case report. American Journal of Case Reports.

Part II.

A) Epidemiology

Of all types of injury, those to the brain are among the

most likely to result in death or permanent disability.
Estimates of traumatic brain injury (TBI) incidence,
severity, and cost reflect the enormous losses to
individuals, their families, and society from these injuries.

▪ The average TBI incidence rate (combined

hospitalization and mortality rate) is 95 per 100,000
population. Twenty-two percent of people who have
a TBI die from their injuries. The risk of having a TBI
is especially high among adolescents, young
adults, and people older than 75 years of age.

▪ It is common among white race.

▪ For persons of all ages, the risk of TBI among males

is twice the risk among females.

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20
▪ The leading causes of TBI are motor vehicle crashes, violence, and falls. Nearly two-thirds of
firearm-related TBIs are classified as suicidal in intent.

▪ The leading causes of TBI vary by age: falls are the leading cause of TBI among persons aged 65
years and older, whereas transportation leads among persons aged 5 to 64 years.

▪ The outcome of these injuries varies greatly depending on the cause: 91% of firearm-related TBIs
resulted in death, but only 11% of fall-related TBIs are fatal.

B) Pathology

Primary traumatic brain injury insult triggers complex

cellular and molecular processes leading to further
neuronal dysfunction and death (secondary injury). It’s
variety of variety of processes involved contributes to the
traumatic brain injury complexity but also creates various therapeutic targets.

This a schematic view of the pathophysiology of secondary cerebral damage after traumatic brain injury
that supports the concept of optimizing cerebral blood flow, the delivery of oxygen and the adequate
supply of energy substrates.

Other features of traumatic brain injury and mechanism following primary onset might include:

▪ Diffuse axonal injury

▪ Degradation of the cytoskeleton

▪ Cortical and subcortical neuronal injury/death

▪ Vascular-related changes (barrier breakdown, vasospasm, oedema)

▪ Haemorrhage 

▪ Ischemia

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20
▪ Glutamate excitotoxicity

▪ Changes in neurotransmitters

▪ Seizures

▪ Physiological disturbances

▪ Free radical generation 

▪ Disruption of calcium homeostasis

▪ Mitochondrial disturbances 

▪ Metabolic disturbances

▪ Altered brain metabolism 

▪ Altered gene expression

▪ Pro-inflammatory state

These events impair cell function impacting movement, memory and learning ability as well as
potentially causing damage to white matter structure.

Vascular Autoregulation: The main mechanism involved in maintaining consistent cerebral pressure
in response to changing systemic arterial pressure are vasoconstriction and vasodilatation of brain
vessels. Traumatic brain injury impairs or even abolishes cerebrovascular autoregulation immediately
after the trauma or over time. 

Ischemia: Cerebral ischemia is a state of decreased blood supply of the brain (hypoperfusion) and
leads primarily to metabolic stress and ionic perturbations.Coexisting traumatic damage such as
structural injury of cell bodies, astrocytes and microglia, cerebral vascular and endothelial damage
intensify the brain tissue damage.

Oedema: it is a common result of traumatic brain injury and can be vasogenic or cytotoxic and can
cause ICP increase and secondary ischemia. 

Neuroinflammation: Damage to blood vessel endothelium following TBI triggers a neuroinflammation

process with a release of cytokines, free radicals, prostaglandins and complements mobilising an active
response from immune system to eliminate the damaged cells and format scar tissue.

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20

C) Diagnostics

Health care providers may use one or more tests that assess a person's physical injuries, brain and
nerve functioning, and level of consciousness in the diagnosis of TBI. Some of these tests are:

Measurements for Level of TBI:

Health care providers sometimes rank

the person's level of consciousness,
memory loss, and GCS score.

Imaging Tests:

Computerized tomography (CT): this process takes X-rays from many angles to
create a complete picture. It can quickly show bleeding in the brain, bruised brain
tissue, and other damage.

Magnetic resonance imaging (MRI): uses magnets and radio waves to produce
more detailed images than CT scans. An MRI likely would not be used as part of an

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20
initial TBI assessment because it takes too long to complete. It may be used
in follow-up examinations, though.

Intracranial pressure (ICP) monitoring: swelling of the brain from a TBI

can increase pressure inside the skull which causes additional damage to
the brain. A health care provider may insert a probe through the skull to
monitor this swelling. In some cases, a shunt or drain is placed into the skull to relieve ICP.

D) Treatment

It is based on the severity of the injury.

Mild injury: this usually require no treatment other than rest and over-the-counter pain relievers to treat
a headache. But, the px usually needs to be monitored closely at home for any persistent, worsening or
new symptoms. He or she may also have follow-up doctor appointments and it's best to limit physical or
thinking (cognitive) activities that make things worse until your doctor advises that it's OK.

Immediate emergency care: this is for moderate to severe traumatic brain injuries focuses on making
sure the person has enough oxygen and an adequate blood supply, maintaining blood pressure, and
preventing any further injury to the head or neck. Treatments in the emergency room or intensive care
unit of a hospital will focus on minimizing secondary damage due to inflammation, bleeding or reduced
oxygen supply to the brain.

Medications: used to limit secondary damage to the brain immediately after an injury may include:

Diuretics-given intravenously to people with traumatic brain injury, help reduce pressure inside the
brain.

Anti-seizure drugs-px who's under moderate to severe traumatic brain injury are at risk of having
seizures during the first week after their injury.

Coma-inducing drugs-used by doctors to put people into temporary comas because a comatose brain
needs less oxygen to function. This is especially helpful if blood vessels, compressed by increased
pressure in the brain, are unable to supply brain cells with normal amounts of nutrients and oxygen.

Surgery: used to address the following problems:

▪ Removing clotted blood (hematomas

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CARUNUNGAN, Karen Crystal J.
BSRT-2
Submitted on: 10/05/20
▪ Repairing skull fractures

▪ Bleeding in the brain

▪ Opening a window in the skull

Rehabilitation:for px who had a significant brain injury will require rehabilitation for them to relearn
basic skills, such as walking or talking.

References:

Mayo Foundation for Medical Education and Research (MFMER).(1998-2020).Retrieved from:

https://www.mayoclinic.org/diseases-conditions/traumatic-brain-injury/diagnosis-treatment/drc-
20378561

Physiopedia(2020). Retrieved from: https://www.physio-

pedia.com/Pathophysiology_of_Traumatic_Brain_Injury

OPENPediatrics. "Introduction to Traumatic Brain Injury" by Lisa DelSignore, MD for OPENPediatrics.

Available from: https://youtu.be/2JNTJKaz-aM

How do health care providers diagnose traumatic brain injury (TBI)?. Retrieved from:
https://www.nichd.nih.gov/health/topics/tbi/conditioninfo/diagnose

Epidemiology of Traumatic Brain Injury.(2015). Retrieved from: https://clinicalgate.com/epidemiology-of-

traumatic-brain-injury/

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