Trauma craneo encefalico Head Trauma.ppt

Trauma neurocirugia

1. Head trauma

2. HT –Head Trauma
HI –Head Injury
CCT -Cranio-cerebral trauma
Abbreviations

3. HT Definition
It is damage of brain (cerebrum, shells of the brain,
vessels, cranial nerves)after action of mechanical
forces on a head

4. HT Epidemiology
In Ukraine 1% from all population have HT
every year
In United States -incidence(number of new
cases) of head injury is
300 per 100,000 per year (0.3% of the
population),
400 000 hospitalizations every year,
75 000 death.
Leading cause of death, ages 15-40.
Major cause of permanent disability.

5. Home
accident HI
65%
Dynamics of Head Injury in agrarian region of Ukraine from 2005 to 2009 yrs. Olkhov
V.M., Chiyka Y.L., Kirichenko V.V., Gorbatuk K.I., Venckovskiy I.L., Olkhova I.V.. 2010

6. Road accident
HI
30%

7. Occupational HI
≈ 1-5%

8. Sport HI
≈ 1-3%

9. Classification of HT
Isolated Multifocal Combined
Injury of the
cerebrum
HT and mechanical
damages of the
other parts of the
body as well
•cranioabdominal
•craniothoracal
•craniofacial
•craniovertebral
•cranioskeletal
HT and the damages
cased by the energy,
that differs from
mechanical one:
•chemical
•radiation
•toxic
•thermic injuries

10. There are no
destruction of the
integrity of a convex
tissues of skull
(aponeurosis)
70%
Damage of the soft
tissues of convex of
the skull (aponeurosis)
30%
Classification of HT
(by possibility of brain tissue infection)
Closed
primary non-infected
Open
primary infected, the
ways for the incoming
of the infection into a
skull
Penetrative
(the dura is damaged)
Non-penetrative
(the dura is not
damaged)

11. Skin
cut
Aponeurosis cut
Bone
cut
Cerebrospinal CSF leakage
Q? What kind of HI is it:
closed, opened, penetrating or not?

12. HT Classification (by severity)
Commotion (Concussion)
Contusion
Compression
DAI (Diffuse Axonal Injury)
Squeezing of the head

13. Clinical forms of damages of the cerebrum
Commotion
Contusion
Defuse axonal
injury (DAI)
Light
severity
Mild
severity
Severe
With
contusion
Without
contusion
Compression
Squeezing of the
head

14. •Commotion
•Light severity contusion
•Mild severity contusion
•Chronic compression of
the cerebrum
•Severe contusion
•Compression of the
cerebrum
•DAI
The severity of the HT
Mild
severity
Middle
severity
Severe

15. Diagnosis of CCT
2.Anamnesis of disease(time, mechanism
of trauma…)
1.General examination.
3.Neurological examination.
4.X-ray of the skull (craniography)
5.Echoencephalography
6.Neurovisualization (CT, MRI)
7.CSF taking through lumbar punction (if no
symptoms of dislocation occur).
8.imposition of diagnostic bore-holes
Obligate examination methods Additive methods
І. Clinical laboratory data
-Blood and urine
-Biochemistry
-CSF
II. Examination of contiguous
doctors
-ophthalmologist
-laryngologist
-traumatologist

16. Clinical display of CCT
1. Common-brain symptoms
(consciousness, headache, nausea,
vomiting, amnesia)
3. Astheno-vegetative syndrome(alteration of
pulsusand AP, hyperhydrosis,
acrocyanosis…)
2. Local neurological symptoms
(permanent or transitory)
4. Dislocation syndrome
4. Meningealsyndrome or meninigism
symptoms (simptoms: Neri, Kernig’s,
Brudzinsky)

17. Consciousness
level
Count:
CL = Eye opening +
Verbal response + Motor
response
Min -3
Max -15

18. Accordance of severity of
HT and consciousness
violation in GCS
Light CCT–13-15 points
Mild severe CCT–9-12 points
Severe CCT–less than 8 points

23. Lumbar puncture
•Severity of HI
•Subarachnoid hemorrhage
•Measurement of ICP
•Liquor labs
•For treatment

24. Mild HT (Concussion/Commotion)

25. Headache
Amnesia, short term memory loss
Vomiting
Blurred Vision
Confusion
Ringing in Ears
Neck Pain
Dizziness
Unconsciousness (Short-term unconsciousness, frequently “immediate” or
from 0 to 20 min)
Irritability
Convulsions
Different vegetative disturbances (increasing of body temperature,
hyperhydrosis, increased fatigue, psychical exhaustion, languor);
Light hearth symptoms, that has the tendency for fast regression during
first days
The life-dependant functions are not violated
Symptoms of a Commotion

26. Diagnosis
The commotion of brain –is a clinical diagnosis, –the
passing through other additive methods of examination
usually shows no alteration in patients status.
Additive methods of examination
General examination with evaluation of
general vital functions(breathing, pulsus, AP).
Neurological examination.
CT of the brain during first 60 min.
X-ray of skull in 2 axis.
Echo-EG(absence of CT).
General laboratory examination.
Coagulation monitoring(from 3d day).

27. Treatment of commotion
of the brain
Dynamic monitoring and prescribing of the strict
bed mode during 7-10 days
Symptomatic treatment (analgesics, sedation, if
necessary –antivomitingpreparations)
Vitamins
In case of unstoppable headache, that does not decrease
after the analgesia, the CSF should be taken with
evaluation of CSF pressure and, dependant on its data, a
proper treatment should be prescribed.

28. HT Contusion
A contusion is a bruise to the brain tissue which
occurs when a number of small blood vessels
leak into brain tissue.
Contusions occur when the brain strikes a ridge
in the skull, when the head moves suddenly or
hits a solid object with great force.

29. Contusion of brain
Contusion of brain –is
more severe damage,
that reflects in
macroscopic
morphological changes
of the brain tissue.

30. Symptoms of a Contusion
Severe Headache
Dizziness
Nausea / Vomiting
Restless, irritable
Memory Loss
Dilated Pupil
Weakness of limbs
Unconsciousness > 20 min

31. Major clinical signs
(symptoms) of contusion of
brain
Common-brain symptoms(generally
long-term unconsciousness),
Permanent hearth symptoms
(depends on region that is
damaged),
Meningealsymptoms (after the
vessels of convex are damaged, the
subarachnoidalhemorrhage
appears).

32. –Unconsciousness (during 10 or more minutes),
–Persistent headache, dizziness, weakness, noise in ears,
–Frequently amnesia appears, expressed nausea, repeating
vomiting,
–Disturbances in vital-depending functions do not appear,
sometimes mild tachycardia or rarely bradycardiaappear,
–Waves of blood to the face, dyssomniaand other vegetative
phenomena,
–Neurological symptoms are frequently “light” (nistagm, light
anisocoria, signs of pyramidal insufficiency, light meningealsigns
and other). Usually neurological symptoms totally regress after 2
or 3 weeks.
Light contusion of brain

33. –Unconsciousness from minutes to hours
–The always amnesia appears,
–Headache is intensive and long-lasting, frequent vomiting, the
psychic alterations are possible
–Disturbances of vital-depending functions (brady-or
tachycardia, increasing of AP, tachypnoewithout changes of
rhythm of breathing, subfibriletemperature, sometimes trunk
violations can occur).
–Meningealsymptoms are frequent and lasting
–The clear hearth symptoms, that determines the zone of
contusion (eye movement violations, paresis of extremities,
violations of sensitivity…), that slowly regress during 2-5 weeks.
Mild contusion of brain

34. –Unconsciousness from hours to several days,
–Psychomotor excitation,
–Severe, frequently threatening to life-dependant functions
neurological symptoms (the trunk symptoms dominate),
–Meningealsymptoms are highly expressed,
–Frequently generalized or focal cramps appear,
–Hearth symptoms regress slowly and untotally, they leave rough
remaining phenomena, foremost from the side of motive and
psychic region.
Severe contusion of brain

38. Diagnostic criteria
X-ray of skull (presence of fracture of skull
bones, presence of foreign objects
witnesses about contusion of brain, even
excluding the clinical data)
CT or MRI
Lumbar punche

39. Indications to surgical treatment of
contusion of brain
Expressed clinical signs of dislocation of brain.
CT (MRI) signs of lateral and axial dislocations of brain.
Signs of growing, resistant to conservative treatment,
intracranial pressure –IP (growing of IP higher than 20-25
mmHg, osmotic pressure of blood plasma lower than 280
mmol/l or higher than 320 mmol/l).

40. Kinds of operative procedures
at contusion of brain
Palliative operations
Punctionof ventricles with positioning of inner ventricular
drainage
Positioning of outer lumbar drainage
CSF shunting
Radical operations
Bone-plastic trepanation, aspiration and washing of brain
detritus
Decompress trepanation

41. HT Compression

42. Compression of brain appears in 3-5% of cases in patients with
CCT, and characterized with fast increasing of common-brain and
hearth symptoms, especially with violations of functions of trunk
of the brain
Compression of brain
Causes of compression of brain in CCT
Formation of intracranial hemorrhage clots (hematoma)
Formation of subdural hydromas,
Pneumocephalia,
Impressed fractures of convex of brain
Foreign objects
Aggressive swallowing of brain, that forms after the brain tissue was
contused

43. A cerebral compression
involves a build up of
pressure on the brain and
can be life threatening,
most often requiring
surgery. Cerebral
compression occurs when
there is an accumulation
of blood within the skullor
injured brain tissue swells
What is a Cerebral Compression

44. Clinical picture of brain compression
In clinical picture of brain compression (first of all by
hematomas) the major symptoms are:
Short period of consciousness after primary lost of it,
Anisocoriawith midriasisat the side of compression,
Bradycardia,
Hemiparesisor hemipalsyon the opposite side of
compression,
Frequently, patients with compression of brain (especially
with impressed fractures and chronic hematomas) have
cramps.

45. Clinical forms of intracranial
hematomas
Depending on the time of manifestation of hematoma, they can
be:
acute—under 3 days;
subacute—under 2 weeks;
chronic—more then 2 weeks.
Varieties of clinical flow:
•Classic flow with short period of
consciousness (lucid interval)
•With erased period of consciousness
•Without period of consciousness
•Without loss of consciousness from start

46. Clinical phases of compression
Phase of clinic compensation(common-brain and hearth symptoms are
absent)
Phase of clinic subcompensation(general conditions of patient is relatively
satisfactory, общее состояние больного относительно удовлетворительное,
he/her is conscious or easy stunned, hearth symptoms are present, dislocation
symptoms are absent, vital functions are not violated).
Phase of mild clinical decompensation(general conditions are mild or severe,
he/her is deeply stunned or soporis present, hearth symptoms increase or new
ones show themselves, there are signs of increased intracranial pressure,
secondary brain trunk symptoms with violations of vital functions appear).
Phase of rough clinical decompensation(general conditions are severe or
extremely severe, coma is present, the signs of compression of brain trunk are
highly expressed, the violation of vital functions become threatening).
Terminal phase.

47. Traumatic epidural hematoma (TEH)
TEH –is caused by trauma accumulation of
blood betweeninner surface of bones of skull
and duramater, frequently in borders of one
bone.
The source of hemorrhage in TEH is the trunk or
one of the branches of a. meningeamedia, or the
branches of meningealartery, rare –veins of dura
mater, duralsinuses or vessels of diploe.
These TEH appear frequently at the
place of placement of traumatic agent.

51. Frequency of TEH depending on their
localization
Topographic and clinical varieties
of TEH
Lateral (typical)TEH
Lobe pole
Temporal pole
Sagital-parasagital
Temporal-basis
Back cranial pit

52. Look
like
Lens

57. TSH–is caused by trauma accumulation of blood between inner
surface of duramater and outer surface of the brain, that causes
the compression of brain.
This kind of haematomasis most frequent (more than half of all the intracranial
haematomas). In a difference from TEH, TSH can form on the opposite side to the
region of placement of traumatic agent, аndin 10-15% of cases they can be at
the both sides.
The source of hemorrhage at TSG are veins, that
flow into the sinuses of brain, superficial vessels
of hemispheres , sometimes damages of sinuses.

58. Rupture of bridging veins

61. Diagnosis
Look
like
Sickle

65. Intracerebral hematoma

67. Subdural hydromas(SH)
SH –is a local accumulation of CSF in subdural space (between
duramater and arachnoidmater of the brain), that caused by
rupturesof arachnoidmater with forming of valve, that allows to
CSF flow only in single direction.
Clinical picture reminds subacuteor chronic TSH and final
diagnosis could be established only after he additive diagnostic
methods are applied, sometimes intraoperative.

69. Foreign objects of brain

70. Foreign objects of brain

71. Foreign objects of brain

72. Foreign objects of brain

73. Foreign objects of brain

74. Non-gunfire
Gunfire Blind 38,5% simple
segmental
radial
diametric
Through-coming4,5% segmental
diametric
Tangential45,9%
rebound11,1%
Kinds of gun-fire lesions of brain

75. Kinds of gun-fire lesions of brain
1.Simple
2.Segmental
3.Radial
4.Diametric

78. Indications to surgical removement of
intracranial haematomas
Clinical signs of compression of brain, even by 1 of criteria:
hearth, common-brain or dislocation symptoms.
Volume of TEH or intracerebralhaematoma(by CT or MRI
data) >50mlfor the supratentorialand >20млfor subtentorial
Thickness of TEH more than 1.5cm, even if it runs without any
symptoms and not depending on clinical phase.
Repeating worsening or decreasing of level of consciousness
after the short term period of consciousness.
Presence of even one sign on CT (MRI) images: lateral
dislocation of median structures >5mm, deformation of basal
cisterns, rough dislocation of homolateralventricle with
dislocativecontralateralhydrocephaly, not depending on the
form and localization of haemotoma.
Haematomasof back cranial pit of low volume (<20ml), if they
cause occlusive hydrocephaly
The presence of even one of described criteria is the direct indication to provide
surgical treatment. Diagnosis, indications and for surgical management and sending
of patient into the operative room should be fulfilled in first 3 hours, counting from
the time of hospitalization.

79. Contraindications to surgical management
Atonic coma with presence of rough brain trunk violations
Verified death of brain
Critical violations of coagulation system (thrombocytopenia –the
number of platelets 50 x 103 mcl and less)
Conservative treatment of intracranial
haematomas (IH)
Stabile, relatively satisfactory status of patient (GCS 15-13 points)
with absence of even minimal hearth and common-brain
symptoms, clinical signs of brain dislocation (by CT, MRI data
under 5mm, without any signs of occlusive hydrocephaly, without
deformation of basal cisterns).
Contraindications for operative treatment may frequently be relative
and surgical management –is the only way to save life of a patient

80. Surgical managment
The surgical tactics consist of next steps:
Trepanation,
Removement of haematoma,
Stop of hemorrhage.
If before the operation localization and size of haematoma verified by CT or
MRI, the bone plastic trepanation is preferred. If such data is absent, the
linear incision of skin should be performed and resection of the bone should
be done.
•In subacute and chronic haematomas, and subdural hydromas the most
adequate surgical approach is removement of them through bore-holes.
•In recent years one of the alternative methods of surgical removement of
some intracranial haematomas is their endoscopic removement.

81. HT Scull Fractures

82. There is a damage of inner
or outer plate only
Kinds of the bone fractures of skull
Untotal
There is a damage of all
layers of the bone
Linear
Splinter
Parceled
Hole-kind
Without dislocation of
the splinters
Impressed fracture
Fractures of basis
Fractures of convex
Concaved

84. Fractures of the bones of skull

95. Diffuse axonal Injury
–Long-lasting coma, that appears immediately after trauma, without the short
period of consciousness
–Symmetrical or asymmetrical symptoms of decerebrationor decortication
–Variety of muscle tonus changes –from diffuse muscular hypotoniato
hormeotonia
–Rough hearth trunk symptoms, meningealsyndrome
–Rough violations of vital-dependant functions, also expressed vegetative
changes
–Coma frequently transforms to transitory or permanent vegetative status, in
case of exit from it, rough violation symptoms last for long time, with
domination of extrapyramidsymptoms and highly expressed violations of
psychic
results as consequence of acceleration-
deceleration + rotation, that lead to total or partial
damage of the axons, frequently combined with small
potted hemorrhages on the regions with max difference
of brain tissue closeness –on the border between grey
and white matter of the brain.

96. HT Emergency Help
1.Evacuation from accident place
2.Call to emergency
3.ABC system assessment
4.Hemostasis
5.Immobilisation of Neck

98. HT Management

102. Removal of chronic subdural
haematoma

112. Consequences of CCT
Postraumatic arachnoiditis
Hydrocephaly, pneumocephaly, porencephaly
Defects and deformations of skull
SCF drainage
Damage of cranial nerves, central paresis and plegia
Scar tissue proliferation on the brain shell
Athrophy of brain(diffuse, local)
Cysts(subarachnoidal, intracerebral)
Epilepsy
Carotide-cavernose junctions
Ischemic damages of brain
Arterial aneurisms of brain
Parkinson's Disease
Psychic and vegetative dysfunctions

120. HT Prognosis

121. Steps in skull defects plastics
X-ray and 3D CT
of skull
Modeling of the
defect region
3D modeling
Producing of self
plate
Surgical
procedure
X-ray after
surgery

122. Plastics of the skull defects