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Head trauma
1. HEAD TRAUMA
Dr. Isa Basuki
Department of Surgery, AWS General Hospital
Faculty of Medicine, MulawarmanUniversity
2. INTRODUCTION
Head trauma orTraumatic brain injury (TBI) is a disruption or alteration of brain
function due to external forces
The external forces creating the injury may be the result of:
acceleration or deceleration,
direct compression,
penetrating objects,
combined effects,
complex mechanisms
3. INTRODUCTION
It may produce:
fractures,
contusion,
subarachnoid hemorrhage (SAH),
subdural hemorrhage (SDH),
epidural hemorrhage (EDH),
Intraparenchymal hemorrhage (IPH),
diffuse axonal injury (DAI).
All injuries and symptoms should be taken seriously
4. EPIDEMIOLOGY
Approximately 1.4 million people per year sufferTBI
1.1 million are treated and released, 240,000 are hospitalized, and 50,000 die
Common causes:
Falls (28%),
Motor vehicle accidents (20%),
Pedestrian impact (19%),
Assault (11%)
Age distribution with the greatest risk in 0–4 and 15- to 19-year-olds.
Males have 1.5 times the risk of females
9. SYSTEMIC EVALUATION AND
RESUSCITATION
Assessment and treatment often begins in the prehospital setting
The basic principles of trauma resuscitation rapid assessment and maintenance
of an airway, breathing, and circulation
medical and surgical history should be obtained including:
the events preceding a trauma,
a description of the accident scene,
accurate description of the patient’s neurological baseline,
any subsequent changes to the neurological status
10. SYSTEMIC EVALUATION AND
RESUSCITATION
In the newborn or premature infant cephalohematoma may allow enough
displacement of blood to produce hemodynamic instability
Raccoon’s eyes (periorbital ecchymosis),
Battle’s sign (postauricular ecchymosis), suggest a basilar skull fracture
otorrhea/rhinorrhea
Puncture wounds penetrating injury to the brain, spinal cord, sympathetic
plexus, or vasculature
Bruits of the carotid artery carotid dissection or carotidcavernous fistula
11.
12. NEUROLOGICAL EXAMINATION
Accurate neurological examination is essential
The exam may be limited due to:
patient’s age
level of education
native language
presence of sedative or paralytic medication
• Illicit drugs
• hypotension
• hypoxia
• hypothermia
• hypoglycemia
13.
14. PUPILLARY RESPONSE
parasympathetic, pupilloconstrictor, and light reflex (pupillary reflex) can be easily
and rapidly assessed in the unconscious patient
Damage to the Edinger–Westphal nucleus or uncal compression of CN III at the
tentorial notch pupillary dilatation (≥4 mm)
Direct orbital trauma can also result in pupillary dilation/fixation in the absence of
temporal lobe herniation or intracranial hypertension (ICHTN).
15. GLASGOW COMA SCALE
standard for objective measurement ofTBI severity
three parameters:
best eye opening [E]
best verbalization [V],
best motor function [M]
GCS = 13 – 15 mildTBI
GCS = 9 – 12 moderateTBI
GCS = 3 – 8 severeTBI
If the patient is intubated 1 for the verbal component and the overall scored is
annotated with a “T.”
Examples: M4/VT/E2 = 4 + 1 + 2 = 7T
20. PLAIN X-RAYS
For evaluating and clearing the cervical spine.
The spine is imaged from the occiput toT1 and a C-collar
AP, lateral and odontoid views are the most useful
T- and L-spine films are obtained based on:
mechanism of injury,
degree of neurological deficits,
pain
21. CT SCAN
CT scan findings after trauma:
SDH, EDH, SAH, IPH, IVH
contusions
hydrocephalus
cerebral edema or anoxia
skull fractures
ischemic infarction (if >12 hours old)
mass effect
midline shift
Indications for an initial post-
traumatic CT scan:
GCS ≤ 14
unresponsiveness,
focal deficit,
amnesia for the injury,
altered mental status,
signs of basilar skull fracture
22. MRI
better parenchymal resolution
can evaluate infarction, ischemia, edema, and DAI
helpful to determine ligamentous injury of the spine or traumatic cord injury
generally performed after the initial trauma evaluation and resuscitation have
been completed
Disadvantages:
limited availability
slower image acquisition time
increased cost
24. SKULL FRACTURES
can be described by:
The state of the overlying scalp (closed or open),
The number of bone fragments (simple or compound),
The relationship of bone fragments to each other (depressed or nondepressed),
Whethert the fracture enters or widens an existing cranial suture (diastatic, more
common in children), and whether it involves the cranial vault or skull base
lower force impacts (falls from standing) more linear, closed, and without dural
laceration
Higher force impacts (MVA, falls from heights, penetrating trauma)
compound, open fractures with underlying dural or cerebral injury
“Ping-pong” fractures are greenstick-type fractures usually seen in newborns
25. CT bone windows showing ping-pong skull
fracture.
The multiple nondisplaced linear lucencies are
normal sutures.
26. SKULL FRACTURES
Associated clinical signs of:
calvarial skull fractures gross deformity and palpable skull fracture in patients with
open scalp lacerations
Basilar skull fractures postauricular or periorbital ecchymosis, hemotympanum or
laceration of the external auditory canal, and CSF rhinorrhea or otorrhea
Cranial nerve injuries:
fractures of the cribriform plate (CN I, anosmia)
optic canal (CN II, visual deficit)
temporal bone (CNVII, facial weakness; or CNVIII, hearing loss)
Severe basilar skull fractures pituitary gland injury endocrinopathies
27. SKULL FRACTURES
Direct injury to vasculature that penetrates the skull base
Arterial dissection,
Traumatic aneurysm formation,
Traumatic carotid-cavernous sinus fistula with symptoms:
cranial neuropathies
chemosis
bruits
Strokes
29. SKULL FRACTURES
RADIOGRAPHIC DIAGNOSIS
Most skull fractures are discovered by CT scan
Plain films may be superior to CT scan in discovering linear calvarial fractures
parallel to the skull base
CT angiograms/venograms to assess
fractures involving skull base foramen containing vasculature (e.g., carotid
canal, foramen magnum)
fractures that cross major venous sinuses (superior sagittal or transverse sinuses, jugular
foramen).
Closed, nondisplaced fractures do not require immediate intervention
Open skull fractures should be debrided and carefully inspected and all should
receive antibiotics
30. SKULL FRACTURES
Relative indications for surgical elevation of a depressed skull fracture:
depression of more than 8–10 mm or more than the thickness of the skull
Focal neurological deficit clearly attributable to compressed underlying brain,
Significant intraparenchymal bone fragments (implying dural laceration),
Persistent deformity after all swelling has subsided
Current recommendations:
surgical repair open fractures depressed greater than the thickness of the cranium
nonoperative management open depressed cranial fractures if there is no evidence
of dural penetration
31. CT bone windows showing a depressed
skull fracture that required surgical
elevation and dural repair.
The patient also had an underlying brain
contusion and presented with a receptive
aphasia
33. FOCAL CEREBRAL INJURIES
CEREBRAL CONTUSION
Injuries to the superficial gray matter of the brain
External forces
acceleration of the intact skull or fractured skull fragments toward the brain surface or
the brain continues to move toward the rapidly decelerating skull and dural folds of the
falx or tentorium
“Coup” lesions ipsilateral to the impact site adjacent calvarial fractures
“Contrecoup” lesions opposite the coup lesion rebounding brain striking the
inner table of the skull
CT scans patchy, hyperdense lesions with a hypodense background
34. FOCAL CEREBRAL INJURIES
INTRAPARENCHYMAL HEMORRHAGE
8.2% of allTBI and up to 35% of severeTBI cases
Delayed traumatic intracerebral hemorrhage (DTICH) approximately 20% of
cases and most occur within 72 hours of the initial trauma
Indications for surgical decompression:
neurological decline referable to theTICH lesion
TICH > 50 cm3
GCS = 6 – 8 with frontal or temporal contusions >20 cm3 with midline shift ≥5 mm and/or
cisternal compression on CT scan
Surgical procedures range
Localized frontal or temporal craniotomy with resection of underlying focal clot
Extensive craniectomies with duraplasty, evacuation of severely contused brain, or
temporal lobectomy
35. FOCAL CEREBRAL INJURIES
EPIDURAL HEMORRHAGE
blood collects in the potential space between the dura and inner table of the skull
1% of all head trauma admissions and in 5–15% of patients with fatal head injuries
more common in males (M:F = 4:1)
usually occurs in young adults
90% of EDHs are due to arterial bleeding fracture at the middle meningeal
artery groove
10% are due to venous bleeding violation of a venous sinus by an
occipital, parietal, or sphenoid wing fracture
36. FOCAL CEREBRAL INJURIES
EPIDURAL HEMORRHAGE
Location of EDH:
lateral convexity of a cerebral hemisphere (70%),
frontal (5–10%),
parieto-occipital (5–10%),
posterior fossa locations (5–10%)
CT scan
hyperdense, biconvex (lenticular) mass adjacent to the inner table of the skull (84%)
medial edge being straight (11%)
crescentic resembling an SDH (5%)
Additional associated findings SDHs and cerebral contusion
37. CT showing epidural hemorrhage. Note the biconvex- or lenticular-shaped hemorrhage.
On the bone windows this was adjacent to a diastatic left lambdoid suture.
38. FOCAL CEREBRAL INJURIES
EPIDURAL HEMORRHAGE
Clinical presentation:
Brief post-traumatic loss of consciousness (LOC) 40%
Lucid interval (80%)
Obtundation
Contralateral hemiparesis,
Ipsilateral (85%) pupillary dilatation (60%)
Kernohan’s phenomenon (a false localizing sign)
local hemispheric mass effect
compression of the contralateral brainstem against the
tentorial notch
ipsilateral hemiparesis
Mortality
unilateral EDH (5–12%)
Bilateral EDH (15–20%)
no lucid interval (20%)
posterior fossa location (25%)
concurrent acute SDH (25–90%)
39.
40. FOCAL CEREBRAL INJURIES
EPIDURAL HEMORRHAGE
Rapid diagnosis and intervention when indicated optimize the outcome
Guidelines:
Surgical EDH of >30 cm3 should be evacuated regardless of GCS score
Conservative EDH of <30 cm3 and <15 mm of thickness and >5 mm midline shift
(frequent neurological examinations and serial CT scan)
Relative indications EDHs that are neurologically symptomatic or have a
maximal thickness >1 cm.
Absolute indication acute EDH in coma (GCS ≤ 8) and anisocoria
Craniotomy complete clot evacuation with meticulous hemostasis and use of
tackup sutures to decrease the potential epidural space
41. FOCAL CEREBRAL INJURIES
SUBDURAL HEMORRHAGE
blood collects between the arachnoid and inner dural layer
Type/variants:
hyperacute (<6 hours),
acute (6 hours to 3 days),
subacute (3 days to 3 weeks),
chronic (3 weeks to 3 months)
Etiologies:
traumatic stretching and tearing of cortical bridging veins
coagulopathy,
subdural dissection of ICH,
rupture of a vascular anomaly (AVM, aneurysm, cavernoma, dural AV fistula) into the
subdural space
42.
43.
44. CT showing an acute subdural hemorrhage. Note that crescentic hemorrhage
crosses under the right coronal suture.
46. FOCAL CEREBRAL INJURIES
SUBDURAL HEMORRHAGE
Guidelines suggestion for SDH evacuation:
acute SDH with thickness >1 cm or a midline shift >5 mm regardless GCS score
acute SDH <1 cm thick and midline shift <5 mm and in coma (GCS ≤8) if:
GCS decreases by 2 points.
pupils that are asymmetric or fixed/dilated.
the ICP ≥20 mm Hg.
Craniotomy ASAP, may require craniectomy and duraplasty for ICP control
Mortality 50% to 90% (related more to the underlying injury, increased in the
elderly and in patients on anticoagulants)
Outcome mortality improvements from 66–90% down to 30–59% if the patient
was operated on in less 4 hours
47.
48. FOCAL CEREBRAL INJURIES
SUBARACHNOID HEMORRHAGE
blood located between the pial and arachnoid membranes
results from venous tears in the subarachnoid space
33% of patients with moderate head injury and is found in nearly 100% of trauma
patients at autopsy.
CT scan sulcal hyperdensity
MRI FLAIR hyperintensity
Clinical presentation headache, emesis, and lethargy
Treatment supportive using IV fluids, anticonvulsants, and nimodipine (to
prevent vasospasm)
49. CT with arrow pointing to a small traumatic subarachnoid
hemorrhage in left central sulcus
53. DIFFUSE CEREBRAL INJURIES
CONCUSSION
Physiological responses transient increase in cerebral blood volume due to loss
of vascular autoregulation
mild cases mild cerebral swelling, or hyperemia
more severe cases malignant cerebral edema elevated ICPs refractory to
nearly all measures and 50–100% mortality “second impact syndrome”
CT scan subtle or nonexistent and include mild diffuse swelling secondary to
hyperemia
Treatment recognition of injury
54. DIFFUSE CEREBRAL INJURIES
DIFFUSE AXONAL INJURY
traumatic axonal stretch injury caused by overlying cerebral cortex and underlying
deep brain structures moving at different relative speeds
Mild axonal stretching + transient neuronal dysfunction
Severe axonal shearing + permanent neuronal damage
80% microscopic and nonhemorrhagic with impaired axonal transport and delayed
axonal swelling
CT scans normal (50–80%) or hyperdense petechial hemorrhage (20–50%)
MRI multifocal hyperintense T2 at frontal lobes (67%), corpus callosum (20%), and
brainstem (10%)
Prognosis generally related to the patient’s age, presenting neurological status, and
trajectory of neurological improvement.
57. MEDICAL MANAGEMENT
Basic measures:
ICU setting with frequent monitoring of:
vital signs,
fluid intake and output
neurological examinations (as permitted)
Multiple invasive lines for:
blood pressure (arterial line),
volume assessment (Swan–Ganz),
administration of fluids, medication, or nutrition (central venous catheter),
urine output or temperature (Foley catheter),
ICP,
cerebral tissue oxygenation, or cerebral blood flow (CBF)
58. MEDICAL MANAGEMENT
kept normothermic and euvolemic with isotonic fluids
GI prophylaxis against Cushing’s (stress) ulcer
head of bed should be elevated to 30–45°
neck should be kept midline
cervical collar and endotracheal tube stabilizer
prevent compression of the jugular veins
promote venous outflow from the head
59. BLOOD PRESSURE AND OXYGENATION
single episode of hypoxemia (apnea, cyanosis or O2 saturation <90% in the
field, or PaO2 < 60 mmHg) or hypotension (SBP < 90 mmHg) predictor of worse
outcome
Oxygen saturation and blood pressure monitoring started in the field and
continued at hospital setting
Goal identifying, avoiding, and rapidly correcting hypoxemia or hypotension
Oxygen administration start as early as possible (may require endotracheal
intubation)
isotonic or hypotonic saline, plasma, colloid, blood, or intravenous pressors to
avoid hypotension
60. INTRACRANIAL PRESSURE ASSESSMENT
modified Monro–Kellie hypothesis
Assuming that the skull is completely inelastic, the ventricular space is confluent
pressures are equally and readily transmitted throughout the intracranial space
balance between the brain, blood volume, and CSF in the intracranial space
Increases in the volume or addition of new components compensatory decreases in
other constituents to maintain the same ICP
Mildly increased, localized pressure in the brain neurological dysfunction of the
immediate area
severe pressure increases local tissue compression, shift of intracranial
structures, subfalcine and transtentorial herniation
most severe compression at the level of the brainstem, occlusion of brainstem
vasculature, infarction, and death.
61.
62. ICP MONITORING
Normal ICPs:
<10–15 mm Hg in adults
3–7 mm Hg in children
1.5–6 mm Hg in infants
ICP monitoring is recommended for:
patients with severeTBI (GCS= 3 – 8)
abnormalCT scan or with severeTBI
considered in patients without an accurate neurological examination due to
sedatives, paralytics, or general anesthesia required
Higher mortality ICP persistently above 20 mm Hg.
63.
64. ANALGESICS AND SEDATIVES
Pain and agitation can cause increased sympathetic tone, increased
temperature, and hypertension
increased venous and ICP,
increased metabolic demand,
resistance to controlled ventilation
may require sedatives or psychotropic medication to prevent self-injurious
behavior and dislodgement of airway, vascular lines, or monitoring equipment
If on ventilators, may require sedatives or paralytics to allow appropriate lung
excursion or timing of breath patterns.
side effects hypotension, alteration or obliteration of the neurological
examination, and rebound ICP elevation
65. ANALGESICS AND SEDATIVES
AGENTS ADVANTAGES
Haloperidol relatively nonsedating quality useful for agitation
fentanyl and its related
derivatives (remifentanil,
sufentanil)
short acting, reversible, and conducive to administration
by continuous infusion for acute and longer-term
analgesia
Midazolam short-acting benzodiazepine effective for sedation of
the ventilatedTBI patient.
Propofol hypnotic anesthetic with rapid onset and a very short half-
life facilitates rapid neurological assessment, reduces
cerebral metabolism and oxygen consumption and exerts
a neuroprotective effect
66. HYPEROSMOLARTHERAPY
Mechanism of Mannitol:
first few minutes produces immediate plasma expansion with reduced hematocrit
and blood viscosity improved rheology, and increased CBF and O2 delivery
reduces ICP
Over the next 15–30 minutes produces an osmotic effect with increased serum
tonicity and withdrawal of edema fluid from the cerebral parenchyma.
Bolus ICP reduction is evident at 1–5 minutes and peaks at 20–60 minutes
Initial bolus of mannitol 1 g/kg
Subsequent administration at smaller doses and longer intervals (i.e., 0.25–0.5
g/kg Q 6 hours)
Furosemide may also be used synergistically with mannitol
67. HYPEROSMOLARTHERAPY
Serum osmolality should be monitored (>320 mOsm/L use of mannitol should
be restricted)
Larger dose (1,4 g/kg) improved outcome of the comatose patients with:
operative subdural hematomas
operative intraparenchymal temporal lobe hemorrhages
abnormal pupillary dilatation
68. HYPERTONIC SALINE
lower ICP through two mechanisms:
1. oncotic pressure gradient, across the BBB, results in mobilization of water from brain tissue and
hypernatremia
2. rapid plasma dilution and volume expansion, endothelial cell and erythrocyte dehydration, and
increased erythrocyte deformability improvements in rheology, CBF, and oxygen delivery
Administration:
continuous infusion of 25–50 mL/h of 3% saline
bolus infusions of 10–30 mL of 7.2%, 10%, or 23.4% saline solution
Onset minutes and may last for hours
Serum sodium and osmolality levels should be aggressively followed central pontine
myelinolysis (most often in patients with preexisting, chronic hyponatremia)
may also induce or exacerbate pulmonary edema in patients with underlying cardiac or
pulmonary deficits
69. HYPERVENTILATION
lowers PCO2 with subsequent vasoconstriction, reduction of cerebral volume, and
reduction in ICP
Time of onset 30 seconds to 1 hour,
Peak effect 8 minutes and may last up to 15–20 minutes
should be avoided during the first 24 hours postinjury CBF is most reduced
after the first 24 hours short-term, mild HPV (PCO2 = 30 – 35) ICP control
moderate HPV should be avoided
Prophylactic HPV (PCO2 ≤ 25) is contraindicated increased ischemia and worse
outcomes
70. DECOMPRESSIVE CRANIECTOMY
The bone is removed, the lesion is resected, and the dura and bone are replaced
Severe cases diffuse cerebral edema, contusions of large size in eloquent areas,
or multiple, coalesced contusions leave the bone flap off.
Most common unilateral hemispheric
Bifrontal and bilateral hemispheric craniectomies based on the location and
severity of the underlying lesion(s)
The dura is opened widely and areas of noneloquent contused and devitalized
brain can be removed if required
hemispheric technique at least 12-cm cranial flap is removed
71. CT of a bilateral hemispheric decompressive craniectomy
performed in a patient with severe edema from a likely
second impact syndrome.
72. BARBITURATES
Benefit:
decreasing metabolic demand for oxygen (CMRO2)
decreasing free radicals and intracellular calcium
lowering ICPs
Side effects:
immunosuppression
hypotension (reduced sympathetic tone and mild cardiodepression)
Patients exclusion:
hemodynamic instability,
sepsis,
respiratory infection,
cardiac risk factors
73. BARBITURATES
loading dose
10 mg/kg over 30 minutes
followed by a 5 mg/(kg h) infusion for 3 hours
maintenance dose 1 mg/(kg h)
Serum barbiturate levels 3–4 mg%
74. HYPOTHERMIA
Improve outcome in patients with
severeTBI through reduction of:
cerebral metabolism,
ICP,
inflammation,
lipid peroxidation,
excitotoxicity,
cell death,
Seizures
Side effects:
Decreased cardiac function
thrombocytopenia
elevated creatinine clearance
pancreatitis
shivering
75. HYPOTHERMIA
patients who were hypothermic on admission had improved outcomes when
hypothermia was maintained
target temperature 32–33°C (maintained for greater than 48 hours)
patients should be closely monitored for electrolyte
abnormalities, hypocoagulability, and cardiac rhythm alterations
Rewarming very slow (not exceeding more than 1° per 24 hours)
76. STEROIDS
Glucocorticoids are not recommended
Side effects of steroid:
coagulopathies,
hyperglycemia,
increased infection
78. NUTRITION
All injured patients show an increase in basal energy expenditure (BEE)
Patients who are sedated and paralyzed 120–130% of baseline
Comatose patients (GCS ≤8) with isolated head injury 140% (range 120–250%)
at least 15% of calories should be supplied as protein
nutritional replacement should start by 72 hours postinjury
Enteral feeding is preferred over parenteral nutrition enhanced
immunocompetence and a reduced risk profile
Total parenteral nutrition
if enteral feeding is not possible
if higher nitrogen intake is required
79. INFECTION
Source of infection:
gross wound contamination
immunosuppression,
iatrogenically from open surgical procedures,
intubation for mechanical ventilation,
invasive monitoring equipment
Antibiotic coverage should be targeted toward specific organisms
Perioperative antibiotics only recommended for the first 24 hours
80. COAGULOPATHY PROPHYLAXIS
Coagulopathies should be rapidly and aggressively treated normal coagulation
profile.
Effects of warfarin anticoagulation may be reversed by:
vitamin K,
fresh frozen plasma (FFP),
prothrombin complex concentrate
Effects of heparin may be reversed with protamine sulfate
Thrombocytopenia or platelet deactivation may be treated with donor platelet
transfusion
81. DVT PROPHYLAXIS
Neurological risk factors for DVT and
PE:
stroke
spinal cord injury,
prolonged surgery
prolonged bed rest
incidence of DVTs in neurosurgical
patients 19% to 50%.
Prophylactic measures
passive range of motion,
early ambulation,
rotating beds,
electrical stimulation of calf muscles
Pharmacologic anticoagulation
increase the effectiveness of DVT
prophylaxis
Low-molecular-weight heparins can
be added to pneumatic compression
boots (PCBs) without significantly
increased risk of hemorrhage
86. PROGNOSIS
Worse prognosis when:
bilaterally dilated (> 4 mm)
absent pupillary light reflexes,
absent oculocephalic or oculovestibular
reflexes,
increased injury severity scale (> 40),
extreme age (> 60 and possibly < 2),
hypotension (SBP < 90 mmHg , worse
with concomitant hypoxemia),
abnormalCT scan (extensive
tSAH, compression or obliteration of
basal cisterns),
persistent ICP > 20 mm Hg,
elevated ICP during the first 24 hours
lower GCS subscores (motor ≤3, eye
opening ≤2, verbal response ≤2)
87. BRAIN DEATH DETERMINATION AND
ORGAN DONATION
Brain death the absence of any observable neurological activity in the brain
and the irreversibility of cessation of the cardiopulmonary system or the entire
brain.
Requirements No complicating conditions:
Hypothermia <32.2°C,
Hypotension [SBP<90]
Exogenous sedatives,
Paralytics
drug/alcohol
Hepatic encephalopathy,
Hyperosmolar coma,
Atropine
Recent CPR/shock/anoxia
88. BRAIN DEATH DETERMINATION AND
ORGAN DONATION
Patient’s condition:
fixed, dilated pupils
no observable corneal, oculocephalic, oculovestibular, gag, or cough reflexes
no movement to deep central or peripheral pain
no spontaneous breathing is seen on disconnection from the ventilator with PaCO2 >60
mm Hg (i.e., apnea test).
Head-injured patients who progress to brain death may be candidates for organ
donation
Organ donation can provide family members with a slightly more positive
conclusion to a series of unfortunate events.
89. REFERENCES
1. Mattox K, Moore E, Feliciano D.Trauma, Seventh Edition. McGraw Hill
Professional; 2012.
2. Jr HRJ Jr, Srinivasan J, Allam GJ, Baker RA. Netter’s Neurology. Elsevier Health
Sciences; 2011.
3. American College of Surgeons, Committee onTrauma. ATLS, advanced trauma
life support for doctors: student course manual. 8th ed. Chicago, IL: American
College of Surgeons; 2008.