SURGERY ASSIGNMENT

The Management Of Head Trauma

Oleh :

No. Nama NPM

1. Putra Dwi Noviono 13700030
2. Theresia Ratnasari Widjaja 13700143
3. Ni Wayan Apriliana Novi A. 13700147
4. Neilavery Winda Suci P. 13700149
5. Galih Setya Budi 13700151
6. Nur Azizah 13700153

MEDICAL FACULTY
WIJAYA KUSUMA UNIVERSITY SURABAYA
2016 2017

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 CHAPTER I

INTRODUCTION

1.1.Background

Injuries are a major public health problem that disproportionately low-

and middle-income countries (LMIC). The most recent World Health

Organizations (WHO) Global Burden of Disease from 2004 reports road

traffic injuries (RTIs), homicides, falls, and other sources of physical injury

account for about 5 million deaths each year with associated permanent

disabilities among the 40 until 50 million survivors. Head injury remains the

most common cause of death following trauma, with particularly high

mortality and morbidity in LMIC. It is estimated that head injury affects 10

million people annually. Due to the poor vital registration infrastructure in

LMIC, WHO mortality statistics are often based on estimates and expert-

derived assumptions (Chandran, 2010). Based on Qureshi (2013) study, 4411

patients were captured within the Swedias KC hospital trauma registry. Of

these, 841 (19%) had head injury and only 201 (24%) of head injured patients

were admitted, and 18 (2%) were dead on arrival (referred to as brought in

dead).

Traumatic brain injury (TBI) is a common, preventable, and disabling

health condition with heterogeneous etiology, type, severity, and outcomes.

Ongoing challenges in TBI care are reflected by rapidly growing literature in

the prevention, assessment and treatment of TBI, especially in sports

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 concussion and blast-related TBI. In comparison, there is a lack of clarity and

standardization in the diagnostic criteria, severity grading, and nomenclature

to describe TBI, which could improve many aspects of TBI care, especially in

developing targeted therapies for TBI. TBI is currently defined as an

alteration in brain function, or other evidence of brain pathology, caused by an

external force. Glasgow Coma Scale (GCS) was introduced for clinical

monitoring following TBI (Teasdale et al., 1974, and was subsequently used

to grade TBI severity (Rimel et al., 1979). Inadequacies of GCS for this latter

purpose is widely recognized, but no clear alternative exists. PTA is an

excellent prognostic marker (Katz et al., 1994), and was incorporated into the

criteria for mild TBI by the American College of Rehabilitation Medicine

(ACRM) (ACRM, 2013). However, there is no consensus in the literature for

the selection of clinical features for TBI diagnosis and severity grading. There

is no standardized nomenclature of TBI subtype, which may be based on the

history, clinical features and imaging findings.

1.2.Problem Formulation

1. What is about Head Trauma which caused Traumatic Brain Injury ?

2. What are clinical symptoms of Head Trauma which caused Traumatic Brain

Injury?

3. How to diagnose Head Trauma which caused Traumatic Brain Injury ?

4. What is the treatment of Head Trauma which caused Traumatic Brain

Injury?

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1.3.Purpose

1. To find out more about Head Trauma which caused Traumatic Brain

Injury?

2. To know clinical symptoms of Head Trauma which caused Traumatic Brain

Injury ?

3. To know how to diagnose Head Trauma which caused Traumatic Brain

Injury ?

4. To find out the treatment of Head Trauma which caused Traumatic Brain

Injury?

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 CHAPTER II

LITERATURE REVIEW

2.1 Definition of Head Trauma

The definition of head trauma is based on a broad definition by Jennett and

MacMillan and includes patients with a history of a blow to the head or the

presence of a scalp wound or those with evidence of altered consciousness

after a relevant injury. The level of consciousness as assessed by the Glasgow

Coma Scale has been used to categorize the severity of a head injury. (SIGN,

2009)

2.2 Definition of Traumatic Brain Injury

TBI is an acute brain injury resulting from mechanical energy to the head

from external physical forces. Operational criteria for clinical identification

include one or more of the following (Ruff,2009):

1. confusion or disorientation

2. loss of consciousness

3. post-traumatic amnesia

4. other neurological abnormalities, such as focal neurological signs, seizure

and/or intracranial lesion.

These manifestations of TBI must not be due to drugs, alcohol or

medications, but caused by other injuries or treatment for other injuries (eg,

systemic injuries, facial injuries or intubation), or caused by other problems

(eg, psychological trauma, language barrier or co-existing medical conditions).

TBI can occur in the context of penetrating craniocerebral injuries but in this

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situation, focal neurological deficits are generally more important than any

diffuse element.

2.3 Degree of head injury GCS score

Mild 13 - 15

Moderate 9 12

Severe 8 or less

(SIGN, 2009)

2.4 Epidemiology

The annual incidence of TBI in the United States has been estimated to

be 180-220 cases per 100,000 population. In the United States, with a

population of almost 300 million, approximately 600,000 new TBIs occur

per year. As many as 10% of these injuries are fatal, resulting in almost

550,000 persons hospitalized annually in the United States with head

injuries. (Ainsworth, 2015).

2.5 Etiology

While various mechanisms may cause TBI, the most common causes

include motor vehicle accidents (eg, collisions between vehicles,

pedestrians struck by motor vehicles, bicycle accidents), falls, assaults,

sports-related injuries, and penetrating trauma.

Motor vehicle accidents account for almost half of the TBIs in the

United States, and in suburban/rural settings, they account for most TBIs.

In cities with populations greater than 100,000, assaults, falls, and

penetrating trauma are more common etiologies of head injury.

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 The male-to-female ratio for TBI is nearly 2:1, and TBI is much

more common in persons younger than 35 years. (Ainsworth, 2015)

2.3 Anatomy of Head Trauma

Several aspects of neuroanatomy and neurophysiology require

review in a discussion of TBI. The brain essentially floats within the CSF;

as a result, the brain can undergo significant translation and deformation

when the head is subjected to significant forces. In a deceleration injury, in

which the head impacts a stationary object, such as the windshield of a car,

the skull stops moving almost instantly. However, the brain continues to

move within the skull toward the direction of the impact for a very brief

period after the head has stopped moving. This results in significant forces

acting on the brain as it undergoes both translation and deformation.

In an acceleration injury, as in a direct blow to the head, the force

applied to the skull causes the skull to move away from the applied force.

The brain does not move with the skull, and the skull impacts the brain,

causing translation and deformation of the brain. The forces that result

from either deceleration or acceleration of the brain can cause injury by

direct mechanical effects on the various cellular components of the brain

or by shear-type forces on axons. In addition to the translational forces, the

brain can experience significant rotational forces, which can also lead to

shear injuries.

The intracranial compartment is divided into 3 compartments by 2

major dural structures, the falx cerebri and the tentorium cerebelli. The

tentorium cerebelli divides the posterior fossa or infratentorial

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compartment (the cerebellum and the brainstem) from the supratentorial

compartment (cerebral hemispheres). The falx cerebri divides the

supratentorial compartment into 2 halves and separates the left and right

hemispheres of the brain. Both the falx and the tentorium have central

openings and prominent edges at the borders of each of these openings.

When a significant increase in ICP occurs, caused by either a large mass

lesion or significant cerebral edema, the brain can slide through these

openings within the falx or the tentorium, a phenomenon known as

herniation. As the brain slides over the free dural edges of the tentorium or

the falx, it is frequently injured by the dural edge.

Several types of herniation exist, as follows: (1) transtentorial

herniation, (2) subfalcine herniation, (3) central herniation, (4) upward

herniation, and (5) tonsillar herniation.

Transtentorial herniation occurs when the medial aspect of the

temporal lobe (uncus) migrates across the free edge of the tentorium. This

causes pressure on the third cranial nerve, interrupting parasympathetic

input to the eye and resulting in a dilated pupil. This unilateral dilated

pupil is the classic sign of transtentorial herniation and usually (80%)

occurs ipsilateral to the side of the transtentorial herniation. In addition to

pressure on the third cranial nerve, transtentorial herniation compresses the

brainstem

Subfalcine herniation occurs when the cingulate gyrus on the

medial aspect of the frontal lobe is displaced across the midline under the

free edge of the falx. This may compromise the blood flow through the

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anterior cerebral artery complexes, which are located on the medial side of

each frontal lobe. Subfalcine herniation does not cause the same brainstem

effects as those caused by transtentorial herniation.

Central herniation occurs when a diffuse increase in ICP occurs

and each of the cerebral hemispheres is displaced through the tentorium,

resulting in significant pressure on the upper brainstem.

Upward, or cerebellar, herniation occurs when either a large mass

or an increased pressure in the posterior fossa is present and the

cerebellum is displaced in an upward direction through the tentorial

opening. This also causes significant upper brainstem compression.

Tonsillar herniation occurs when increased pressure develops in

the posterior fossa. In this form of herniation, the cerebellar tonsils are

displaced in a downward direction through the foramen magnum, causing

compression on the lower brainstem and upper cervical spinal cord as they

pass through the foramen magnum.

Another aspect of the intracranial anatomy that has a significant

role in TBI is the irregular surface of the skull underlying the frontal and

temporal lobes. These surfaces contain numerous ridges that can cause

injury to the inferior aspect of the frontal lobes and the temporal lobes as

the brain glides over these irregular ridges following impact. Typically,

these ridges cause cerebral contusions. The roof of the orbit has many

ridges, and, as a result, the inferior frontal lobe is one of the most common

sites of traumatic cerebral contusions (Ainsworth, 2015)

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2.4 Pathophysiology of Head Trauma

A blow to the head causes its injury basically by putting excessive

strain on the brain and supporting tissues. The scalp can be lacerated, the

skull can be fractured, or a hematoma can form from torn blood vessels.

These can occur in the scalp, under the galeal aponeurosis (subgaleal),

between the dura and skull (epidural), between the dura and arachnoid

(subdural), or in the brain (intracerebral). Contusions (bruises) can occur

on the cortical surfaces. Such focal damage can occur at the point of

impact or frequently on the opposite pole of the brain along the force line

(contrecoup). The contrecoup injury is most frequently seen in

deceleration injuries where the moving head strikes a stationary object

(e.g., when a patient falls and the head hits the floor). Subarachnoid blood

is usually present, and widespread damage can also occur throughout the

white matter. These white matter lesions are due to the shearing forces

initiated by the brains rapid acceleration (when the head is struck) or

deceleration (when the moving head hits a stationary surface). The major

damage to the brain seems to be caused by the rather free rotational and

lateral motion of the brain within the skull. This motion allows the brain to

move against rough surfaces of the base of the skull and also to twist and

distort itself. It is these distortional forces and movement that produces the

strain and stretching of axons and vessels. (SIGN, 2009)

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2.3. Symptoms of Head Trauma

A. Symptoms

As a type of organ system failure, brain failure invariably affects

consciousness. Consciousness is structurally produced in the cerebral

hemispheres, including the pons and the medulla. These structures are all

interconnected by the reticular formation, which begins in the medulla

and extends to the midbrain, where it forms the reticular activating

system. This pathway modulates the perception of events and controls

integrated responses.

Clinical evaluation of consciousness states is heavily dependent on

the findings from the physical examination. When the physical

examination yields visual and palpable clues to the integrity of

consciousness, impairment thereof may be classified into one of the

following categories:

1. Cloudy consciousness: This state is defined as a mild deficit in the

speed of information processing by the brain. This results from

macrotearing and histological-level disruption of cell-to-cell connectivity

occurring throughout the brain disrupting physical connectivity between

brain regions, exacerbated by vascular compromise of a mechanical and/or

biochemical nature causing islands of nonfunctional or impaired tissue in

the brain parenchyma. Cloudy consciousness may be noted after mild-to-

moderate head trauma and may persist for several months. Memory of

recent events is often diminished, but long-term memory typically remains

intact.

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 2. Lethargy: This state is defined as a decrease in alertness, resulting in

impaired ability to perform tasks that are normally accomplished without

effort. Patients rouse briefly in response to stimuli and then settle back

into inactivity when left alone. They retain awareness of their immediate

environment.

3. Obtundation: This state is defined as a decrease in awareness and

alertness, in which patients rouse briefly in response to stimuli and

follow simple commands but are unaware of their immediate

surroundings. When stimulation ceases, they settle back into inactivity.

4. Stupor: In this state, patients cannot communicate clearly but can be

aroused by continued painful stimulation. Arousal may be manifested

only as withdrawal from painful stimuli. As soon as stimuli are removed,

the patient settles back into inactivity.

5. Coma: In this state, patients do not respond to even the most

vigorous stimuli.

6. Brain death: This state is equivalent to functional decapitation and is

characterized by irreversible cessation of whole-brain function and

hemisphere and brainstem function.

The efficacy of the physical examination in the evaluation of

consciousness diminishes when visual clues disappear (eg, during heavy

sedation, therapeutic musculoskeletal paralysis). In such situations,

monitoring of cerebral function by compressed spectral array is helpful in

assessing the effect of therapy on neuronal function. (Ainsworth, 2015)

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 B. Possible Causes of Head Trauma

Motorcycle-related head injuries deserve special mention.

Motorcycle rights organizations dedicated to promoting safety and to

preserving individual freedom suggest that safety should be a choice rather

than a requirement; safety is a good choice, but individual motorcyclists

should have the right to make a bad choice that ends in disaster if they so

choose. A hallmark of the antihelmet movement is the argument that

motorcyclists who do not wear helmets can perceive (ie, see and hear)

their environment more effectively and, thus, can avoid impending

accidents by anticipating them earlier. This argument is fallacious.

Most accidents involving adult, otherwise responsible,

motorcyclists are caused by moving objects hitting motorcyclists or by

motorcyclists hitting a stationary object after being forced into an unusual

position in an attempt to avoid something in their path. A full-face helmet

restricts a relatively small portion of inconsequential downward and lateral

peripheral vision. Similarly, it is highly improbable that a motorcyclist will

hear an impending accident. A marginal increase in the ability to hear road

noise and to see downward and laterally is not an improvement in the

ability to avoid most accidents. (Ainsworth, 2015)

2.4. Diagnosis of Head Trauma

There is no gold standard for the diagnosis of TBI, as some

forms of radiological imaging are neither sensitive nor specific for TBI.

There are also instances where individuals who do not meet low-

threshold criteria for the diagnosis of TBI (those with no loss of

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 consciousness, with a normal Glasgow Coma Scale score and no

amnesia) have evidence of injury to the brain, such as a contusion, The

CT/MRI scan has revolutionized the evaluation of head trauma patients.

CT scans can readily identify the presence of most intracranial injuries

including hematomas, contusions, tissue ischemia, mass effect, edema,

and hydrocephalus. CT scanning will not demonstrate white matter

shearing injuries, which are seen more clearly with MRI. (Weisberg,

2013)

2.4 Treatment of Head Trauma

Treatments for TBI patients are varied and complex. Evidence to support

early rehabilitation interventions for definable stages of recovery for patients

emerging from traumatic coma (such as, early application of awareness

stimulation techniques), and management of PTA (reducing agitation by

environmental modification) is unclear. Treatments for TBI address

cardiovascular disorders (e.g. hypertension); respiratory issues; fever; bladder

and bowel dysfunction; swallowing and nutrition; and spasticity management.

Others target thrombophlebitis; contractures; fractures; peripheral nerve

injuries; and heterotopic ossification. Despite a range of cognitive remediative

therapies that are cornerstone of rehabilitation, and specific interventions for

movement disorders in TBI (such as tremors, rigidity, dystonia, chorea, or tics),

the evidence to support these interventions needs clarification. The objectives

of this overview are to critically examine the literature for diagnostic criteria,

severity grading, and types of TBI, to present existing evidence for treatment in

TBI, and to consider future direction in TBI diagnosis and management.

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 The purpose of head trauma treatments is to prevent, control, or diminish

intracranial hypertension, regardless of its cause. In addition to mass lesions,

acute brain swelling (a vascular engorgement phenomena) and brain edema can

complicate any primary brain injury by causing or aggravating intracranial

hypertension. It is for this reason that, optimally, neurosurgical consultation

should be obtained when these measures are instituted.

a. Induced hypocapnia

Arterial carbon dioxide concentration profoundly affects cerebral

circulation. When abnormally elevated, cerebrovasodilatation occurs,

increasing intracranial blood volume and intracranial pressure. (See II.

Anatomy and Physiology, H. Intracranial Pressure in this chapter.)

Conversely, reduction of PaCO2 reduces intracranial blood volume and,

secondarily, intracranial pressure. Additionally, hyperventilation tends

to reduce intracerebral acidosis and increase cerebral metabolism, both

of which are beneficial. Therefore, hyperventilation is recommended to

reduce arterial PaCO2, maintaining it at 26 to 28 mm Hg. This

procedure usually requires endotracheal intubation, controlled

ventilation, and intermittent iatrogenic paralysis. Intubation should be

performed early for the comatose patient. Care must be taken to assure

that injudicious intubation does not cause further intracranial problems

due to increased intracranial pressure elevations from coughing or

gagging during intubation. Continued intubation may require sedation or

iatrogenic paralysis. Hypocapnia can reduce cerebral circulation to the

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 point where cerebral ischemia occurs. Blood gases must be monitored

closely.

b. Fluid control

Intravenous fluids should be administered judiciously to prevent

overhydration, which augments cerebral edema. since the nature and

volume of fluids administered will depend on the systemic status of the

patient, consultations between the trauma surgeon and the neurosurgeon

are necessary. Intravenous fluid used for maintenance must not be

hyposmolar, as cerebral edema may likewise follow.

c. Diuretics

Diuretics such as mannitol, which cause diuresis by producing

intravascular hyperosmolarity, are widely used for severe brain injury.

Mannitol undoubtedly can be very 20 effective in shrinking brain

volume and lowering intracranial pressure. However, other effects may

cause major problems. In the emergency department, this agent should

be administered only with the consent of a neurosurgeon or to gain time

when neurosurgical capabilities will be delayed and the patient's

condition is deteriorating. Mannitol is most commonly and effectively

used for a suspected surgical mass lesion when time is needed to prepare

for operation (ie, hematoma with deteriorating level of consciousness,

hemiparesis, and dilating pupil). For the average patient, 1 g/kg, is

administered rapidly and intravenously. Care must be taken to prevent

subcutaneous infiltration. The neurosurgeon also may recommend loop

diuretics, such as furosemide, (40 to 80 mg IV for adults). These

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 medications act by medically decompressing the brain and may buy up

to several hours of reduced intracranial pressure. A urinary catheter is

required. Because of the rapid production of urine, vascular volume may

be significantly affected. Therefore, the patient's blood pressure must be

closely monitored, especially if the patient has sustained multiple trauma

or is a child. Urine volume may be replaced with isotonic fluids in these

patients.

d. Steroids

Steroids are not recommended for the treatment of acute head injury

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 CHAPTER III

DISCUSSION

3.1 Anamnesis

Inquire specifically about each symptom or area of symptoms below, since

individuals with TBI may have difficulty organizing and communicating their

symptoms without prompting. It is important to document all problems, whether

subtle or pronounced, so that the veteran can be appropriately evaluated for all

disabilities due to TBI. Also document all negative responses.For each of the

following symptoms that is present, answer specific questions asked.

a. headaches - frequency, severity, duration, and if they most resemble

migraine, tension-type, or cluster headaches

b.dizziness or vertigo - frequency

c. weakness or paralysis - location

d.sleep disturbance - type and frequency

e. fatigue - severity

f. malaise

g.mobility - state symptoms

h.balance - state any problems

i. if ambulatory, what device, if any, is needed to assist walking?

j. memory impairment - mild, moderate, severe

k.other cognitive problems Y/N? If yes, which?:

l. Decreased attention, Difficulty concentratingDifficulty with executive

functions (speed of information processing, goal setting, planning,

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 organizing, prioritizing, self-monitoring, problem solving, judgment,

decision making, spontaneity, and flexibility in changing actions when they

are not productive)

m. speech or swallowing difficulties - severity and specific type of problem -

expressive aphasia?, difficulty with articulation because of injuries to

mouth?, aspiration due to difficulty swallowing?, etc.

n.pain - frequency, severity, duration, location, and likely cause

o.bowel problems - extent and frequency of any fecal leakage and frequency

of need for pads, if used; need for assistance in evacuating bowel (manual

evaluation, suppositories, rectal stimulation, etc.) - report type and frequency

of need for assistance.

3.2 Physical Examination

A. Inspection

The physical exam begins with a general overview of the patient looking for

evidence of scalp trauma, skull fractures, or signs of basilar skull fracture

(characteristic ecchymosis, or CSF otorrhea or rhinorrhea). The ecchymosis found

with basilar skull fractures such as bilateral periorbital bruising (raccoon's eyes) or

bruising over the mastoid area (Battle's sign) are rarely present acutely and may

take hours to develop. Subtle findings such as external ear canal laceration or

hemotympanum may direct additional testing.

B. Palpation

1. Motor function. Report the motor strength of the affected muscles of all
areas of weakness or paralysis using the standard muscle grading scale,

19
 for example, weakness of flexion of left elbow (3/5 strength for flexors),
complete paralysis of left lower extremity (0/5 for all muscle groups).
2. Muscle tone, reflexes. Describe any muscle atrophy or loss of muscle
tone. Examine and report deep tendon reflexes and any pathological
reflexes.
3. Sensory function. Describe exact location of any area of abnormal
sensory function. State which modalities of sensation were tested.
Identify the peripheral nerve(s) that innervate the areas with abnormal
sensation.
4. Cranial nerves. Conduct a screening exam for cranial nerve impairment.
If positive, follow Cranial Nerves examination protocol.
5. Cognitive impairment. Conduct a screening examination (such as the
Montreal Cognitive Assessment (MOCA) or Mini-Mental State
Examination (MMSE)) to assess cognitive impairment and report results
and their significance.
3.3 Additional Examination

1. Skull roentgenograms

Skull roentgenograms are of little value in the early management of

patients with obvious head injuries, except in cases of penetrating injuries. The

unconscious patient should have skull roentgenograms only if precise care of the

cardiorespiratory system and continuing reassessment can be assured. Physical

examination is usually more valuable than skull roentgenograms. Clinical signs of

basal fractures are more useful than roentgenograms of the skull base in

diagnosing a fracture. Increasingly, skull films are not being obtained on patients

with minor head injuries because the information obtained is rarely helpful one

way or the other. When in doubt about the patient's condition, the physicians

should obtain neurosurgical consultation.

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 2. Computed tomography

The CT scan has revolutionized diagnosis in patients with head injuries

and is the diagnostic procedure of choice for patients who have or are suspected of

having a serious head injury. Although not perfect, the CT scan is capable of

showing the exact location and size of most mass lesions. Specific diagnosis

allows more precise planning of definitive care, including operation. The CT scan

has supplanted less specific and more invasive tests, such as cerebral angiography.

Except for patients with minor head injuries, all head-injured patients will require

CT scanning at some time. The more serious the injury, the earlier and more

emergent is the need for the scan. Consequently, injured patients seen first at

facilities without CT capability may require transfer to more sophisticated

hospitals. Once initial resuscitation has been undertaken and the need for a CT

scan determined, care must be taken to (1) maintain adequate resuscitation during

the scan, and (2) assure the 10 best possible quality of the scan. However, efficient

and correct management of the patient, in certain situations, may dictate

otherwise.

3. Other tests

Lumbar puncture, electroencephalogram, and isotope scanning have no

role in the acute management of head trauma. Certain reflexes, eg, oculocephalic

and vestibulo-ocular, can reflect the integrity of a portion of the brain-stem neural

pathways. Although these may permit more specific diagnosis in some instances,

their elicitation can be hazardous, their interpretation difficult, and they add little

21
to the emergency management of the patient. They are best left to the

neurosurgical consultant.

3.4 Treatment

1. Assessing the need for surgery

Injuries requiring surgery are likely to occur in different circumstances than

injuries not requiring surgery. Therefore, a gross estimate of a patient's potential

need for surgery can be based on knowledge concerning three factors:

(1) whether the patient is comatose;

(2) whether the trauma was vehicular or nonvehicular; and

(3) whether there is a lateralized motor deficit.

2. Maintenance of cerebral metabolic needs

Cerebral ischemia or hypoxia result in insufficient substrate delivery to the

injured brain. These conditions are present in more than 90% of patients who die

of head trauma, are associated with poor outcome, and are the most important

preventable complications of head injury. The principal metabolic requirements of

the brain are oxygen and glucose, which are normally used at extremely high

rates. The injured brain usually has a lowered cerebral metabolism and therefore

requires less oxygen and glucose. However, the damaged brain is more

susceptible to the lack of these substrates, and thus temporary severe or prolonged

moderate deprivation causes worse damage than in the uninjured brain. Therefore,

emergency management of head injury includes maintenance of adequate cerebral

22
metabolic fuels. The physician must assure delivery of adequate levels of glucose

and oxygen to the brain. Delivery of these substrates depends on their arterial

concentrations and the blood flow to the brain. Blood glucose concentration is not

a common problem in trauma, but if it is, correction with supplemental

intravenous glucose is needed. However, recent works suggest that hyperglycemia

should be avoided.

3. Preventing / treating intracranial hypertension

The purpose of these treatments is to prevent, control, or diminish intracranial

hypertension, regardless of its cause. In addition to mass lesions, acute brain

swelling (a vascular engorgement phenomena) and brain edema can complicate

any primary brain injury by causing or aggravating intracranial hypertension. It is

for this reason that, optimally, neurosurgical consultation should be obtained

when these measures are instituted.

3.5 Prognosis

In a retrospective series of 846 patients with severe TBI (GCS of 8 or less)

reported by Jiang et. al. one-third of patients had either died or remained in a

persistent vegetative state at one year following their injury. However, 31.56% of

individuals still experienced a good recovery defined as the ability to live

independently and return to work or school. These data highlight the difficulty

with accurate prediction of individual patient prognosis in TBI. (Ainsworth,

2015).

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 CHAPTER IV

CONCLUSSION

3.1. Conclusion

TBI is an acute brain injury resulting from mechanical energy to the head

from external physical forces. The most common cause the TBI is motor vehicle

accidents and TBI is much more common in persons younger than 35 years.

There is no gold standard for the diagnosis of TBI, as some forms of

radiological imaging are neither sensitive nor specific for TBI. But CT scans can

readily identify the presence of most intracranial injuries including hematomas,

contusions, tissue ischemia, mass effect, edema. The treatment are Assessing the

need for surgery, maintenance of cerebral metabolic needs, preventing / treating

intracranial hypertension. In a retrospective series of 846 patients with severe TBI

(GCS of 8 or less) reported by Jiang et. al. one-third of patients had either died or

remained in a persistent vegetative state at one year following their injury.

However, 31.56% of individuals still experienced a good recovery defined as the

ability to live independently and return to work or school

24
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