Head Injury

From ATLS Chapter 6

Marselno Tatipikalawan
Anatomi
 The primary goal of treatment for patients with suspected TBI is
to prevent secondary brain injury.
 The most important ways to limit secondary brain damage and
thereby improve a patient’s outcome are to ensure adequate
oxygenation and maintain blood pressure at a level that is
sufficient to perfuse the brain
 CT scanning should not delay patient transfer to a trauma center
that is capable of immediate and definitive neurosurgical
intervention
Intracranial
compartements
 The tentorium cerebelli divides the intracranial cavity into the
supratentorial and infratentorial compartments
 The midbrain passes through an opening called the tentorial
hiatus or notch
 The oculomotor nerve (cranial nerve III) runs along the edge of
the tentorium and may become compressed against it during
temporal lobe herniation
 Parasympathetic fibers that constrict the pupils lie on the surface
of the third cranial nerve; compression of these superficial fibers
during herniation causes pupillary dilation due to unopposed
sympathetic activity
Sumber: https://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/tentorium-cerebelli
  The normal ICP for patients in the resting state is approximately
10 mm Hg. Pressures greater than 22 mm Hg, particularly if
Intracranial sustained and refractory to treatment, are associated with poor
outcomes
Pressure &  The doctrine states that the total volume of the intracranial
Monroe-Kellie contents must remain constant, because the cranium is a rigid
container incapable of expanding
doctrine  When the normal intracranial volume is exceeded, ICP rises.
Venous blood and CSF can be compressed out of the container,
providing a degree of pressure buffering
  For clinical purposes, cerebral perfusion pressure (CPP) is defined
as mean arterial blood pressure minus intracranial pressure (CPP
= MAP – ICP
 A MAP of 50 to 150 mm Hg is “autoregulated” to maintain a
Cerebral Blood constant CBF (pressure autoregulation)

Flow  In this situation, if the MAP is too low, ischemia and infarction
result.
 If the MAP is too high, marked brain swelling occurs with
elevated ICP.
Classification of
Head Injury
  Skull fractures can occur in the cranial vault or skull base.
 Basilar skull fractures usually require CT scanning with bone-
window settings for identification
 Clinical signs of a basilar skull fracture include periorbital
ecchymosis (raccoon eyes), retroauricular ecchymosis (Battle’s
Skull Fractures sign), CSF leakage from the nose (rhinorrhea) or ear (otorrhea),
and dysfunction of cranial nerves VII and VIII (facial paralysis and
hearing loss), which may occur immediately or a few days after
initial injury.
 Do not underestimate the significance of a skull fracture, because
it takes considerable force to fracture the skull
  Are classified as diffuse or focal
 Diffuse brain injuries range from mild concussions, in which the
head CT is normal, to severe hypoxic, ischemic injuries.
Intracranial  Another diffuse pattern, often seen in high-velocity impact or
deceleration injuries, may produce multiple punctate
lesion hemorrhages throughout the cerebral hemispheres.
 These “shearing injuries,” often seen in the border between the
gray matter and white matter, are referred to as diffuse axonal
injury (DAI)
  Focal lesions include epidural hematomas, subdural hematomas,
contusions, and intracerebral hematomas

Intracranial
lesion
  Epidural hematomas are relatively uncommon, occurring in
about 0.5% of patients with brain injuries and 9% of patients with
TBI who are comatose
 They are most often located in the temporal or temporoparietal
Epidural regions and often result from a tear of the middle meningeal
artery due to fracture
hematoma  they also may result from disruption of a major venous sinus or
bleeding from a skull fracture.
 The classic presentation of an epidural hematoma is with a lucid
interval between the time of injury
  They often develop from the shearing of small surface or bridging
Subdural blood vessels of the cerebral cortex
 Damage from an acute subdural hematoma is typically much
hematoma more severe than that associated with epidural hematomas due
to the presence of concomitant parenchymal injury
  Most contusions are in the frontal and temporal lobes, although
they may be in any part of the brain
Contusions and  In a period of hours or days, contusions can evolve to form an
intracerebral hematoma or a coalescent contusion with enough
intracerebral mass effect to require immediate surgical evacuation
hematomas  For this reason, patients with contusions generally undergo repeat
CT scanning to evaluate for changes in the pattern of injury within
24 hours of the initial scan
Management
of TBI
Management
of TBI
Management
of TBI
  The secondary survey is particularly important in evaluating
patients with mild TBI
 Note the mechanism of injury and give particular attention to
Management any loss of consciousness, including the length of time the patient
was unresponsive, any seizure activity, and the subsequent level of
of mild TBI alertness
Management
of mild TBI
Management
of mild TBI
  Approximately 15% of patients with brain injury who are seen in
the ED have a moderate injury. These patients can still follow
Management simple commands,
of moderate  but they usually are confused or somnolent and can have focal
neurological deficits such as hemiparesis.
TBI  serial neurological examinations are critical in the treatment of
these patients
Management
of moderate
TBI
  All patients with moderate TBI require observation
Management  Frequent neurological reassessment for at least the first 12 to 24
hours
of moderate
 A follow-up CT scan within 24 hours is recommended if the initial
TBI CT scan is abnormal or the patient’s neurological status
deteriorates.
  A “wait and see” approach in such patients can be disastrous, and
Management prompt diagnosis and treatment are extremely important.

of severe TBI  Do not delay patient transfer in order to obtain a CT scan.

Management
of severe TBI
Management
of severe TBI
  Maintain systolic blood pressure (SBP) at ≥ 100 mm Hg for
Management patients 50 to 69 years or at ≥ 110 mm Hg or higher for patients 15
to 49 years or older than 70 years; this may decrease mortality
of severe TBI and improve outcomes
  to prevent secondary damage to an already injured brain
 The basic principle of TBI treatment is that, if injured neural tissue
Medical is given optimal conditions in which to recover, it can regain
normal function.
Therapies for
 Medical therapies for brain injury include intravenous fluids,
TBI correction of anticoagulation, temporary hyperventilation,
mannitol (Osmitrol), hypertonic saline, barbiturates, and
anticonvulsants.
  Hypovolemia in patients with TBI is harmful.
 Clinicians must also take care not to overload the patient with
Intravenous fluids, and avoid using hypotonic fluids.
 Moreover, using glucose-containing fluids can cause
fluid hyperglycemia, which can harm the injured brain.
 Ringer’s lactate solution or normal saline is thus recommended for
resuscitation
Correction of
anticoagulation
  Normocarbia is preffered
 Acts by reducing PaCO2 and causing cerebral vasoconstriction
 Use hyperventilation only in moderation and for as limited a
period as possible.
Hyperventilation
 In general, preferable to keep PaCO2 at approx 35 mmHg
 Hyperventilation will lower ICP in a deteriorating patient with
expanding intracranial hematoma until doctors can perform
emergent craniotomy.
  Mannitol (Osmitrol) is used to reduce elevated ICP
 The most common preparation is a 20% solution (20 g of
mannitol per 100 ml of solution).
 Acute neurological deterioration—such as when a patient under
observation develops a dilated pupil, has hemiparesis, or loses
Mannitol consciousness  strong indication for administering mannitol
 In this case, give the patient a bolus of mannitol (1 g/ kg) rapidly
(over 5 minutes) and transport her or him immediately to the CT
scanner/OR
  Hypertonic saline is also used to reduce elevated ICP, in
Hypertonic concentrations of 3% to 23.4%; this may be the preferable agent
saline for patients with hypotension, because it does not act as a
diuretic.
  Barbiturates are effective in reducing ICP refractory to other
measures, although they should not be used in the presence of
Barbiturat hypotension or hypovolemia
  Anticonvulsants can inhibit brain recovery, so they should be used
only when absolutely necessary
 Loading dose is 1 g of phenytoin intravenously given no faster
Anticonvulsant than 50 mg/min. Maintenance dose 100g/8 hours
 Valium (Diazepam) or ativan (Lorazepam) is frequently used in
addition to phenytoin until the seizure stops
Surgical  Surgical management may be necessary for scalp wounds,
depressed skull fractures, intracranial mass lesions, and
management penetrating brain injuries.
Brain Death
 Glasgow Coma Scale score = 3
 Nonreactive pupils
“  Absent brainstem reflexes (e.g., oculocephalic,corneal, and doll’s
eyes, and no gag reflex)
A diagnosis of brain death
implies that there is no  No spontaneous ventilatory effort on formal apnea testing
possibility for recovery of
brain function  Absence of confounding factors such as alcohol or drug
intoxication or hypothermia
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