This document summarizes a seminar on head injuries presented by Dr. Soumen Kanjilal. It discusses the anatomy of the skull and meninges, types of head injuries including concussions, contusions, extradural and subdural hemorrhages. It covers the management of traumatic brain injuries including indications for CT scans, initial management, treatment of elevated intracranial pressure, and intensive care management. Diffuse axonal injury is also summarized.

1. A SEMINAR ON HEAD
INJURY
PRESENTED BY:
Dr. SOUMEN KANJILAL (2ND YR PGT)
MODERATED BY:
Dr. P.P. DHAR (Asstt. Prof., Deptt. of SURGERY)

2. Basic anatomy
• Skull
• Meninges
• Dura Mater
• Arachnoid
• Pia Mater
• Brain Tissue
• CSF and Blood

3. Meningeal Layers:
Dura mater
Arachnoid
Pia mater
Meningeal Spaces:
Epidural – contains
meningeal
arteries & veins
Subdural – traversed by
“bridging”veins
Subarachnoid -
communicates
with ventricles, includes
cisterns, contains CSF,
circle of Willis.

4. INTRACRANIAL VOLUME
80%
Brain Matter
10%
Blood
10%
CSF

5. What is Traumatic Brain Injury?
• Traumatic Brain Injury (TBI)
occurs when a sudden trauma
damages the brain causing
bleeding, bruising, or tearing of
nerves.

6. What are causes of TBI?
• Motorcycle or Motor vehicle
crashes (RTA)
• Falls
• Violence
Gun shots
Abuse
• Explosive blasts
Military personnel

7. How a patient with Head Injury presents??
• Physical symptoms
• Unconsciousness
• Severe headache
• Repeated nausea and vomiting
• Dizziness
• Seizures
• Weakness
• Numbness in arms and legs
• Dilated pupils of the eye
• Psychological symptoms
• Slurred speech
• Confusion
• Agitation
• Memory or concentration
problems
• Amnesia about events prior to
injury

8. The MONROE KELLIE doctrine

9. Mass effect of HEMATOMA
When decompensated
•Raised ICP
•Hypoxia
•Herniation
CPP = MAP - ICP

10. HERNIATION
1. Herniation of Cingulate Gyrus
(sub-falcine herniation)
2. Herniation is associated with midline
shift.
3. Herniation of the uncus of the
temporal lobe
-Associated with compression of the
ipsilateral 3rd Nerve
4. Central herniation
5. Tonsillar herniation
Associated with compression of brain
stem structures.

11. NEUROSURGICAL EXAMINATION IN TRAUMA
• GENERAL PHYSICAL CONDITION

12. continued…….
2. Cranio- cervical auscultation:
A. Over carotid arteries: bruit may be associated with carotid dissection.
B. Over globe of eye: bruit may indicate traumatic carotid-cavernous fistula.
3. Physical signs of trauma to spine: bruising, deformity.
4. Evidence of seizure: single, multiple or continuing (status epilepticus)

13. NEUROLOGIC EXAMINATION
1. CRANIAL NERVE EXAMINATION
A. Optic nerve function
 if conscious: serial quantitation of vision in each eye is important.
(children may develop transient cortical blindness lasting 1-2 days, usually after a blow to the back
of the head)
 If unconscious: afferent pupillary defect should be looked for. (swinging flash-light)
 Fundoscopic examination: papilledema, pre-retinal hemorrhage, retinal detachment, etc.
B. Pupil: size, reaction to light ( both direct and consensual)
C. VII nerve palsy
D. VI nerve palsy: seen in increase ICP.
2. LEVEL OF CONCIOUSNESS/ MENTAL STATUS : Glasgow Coma
Scale Score
3. MOTOR EXAMINATION
4. SENSORY EXAMINATION
5. REFLEXES: DTR, plantar reflex

15. CATEGORISATION OF HEAD INJURY SEVERITY
CATEGORY CRITERIA
MINIMAL
MILD Or
MODERATE
Or Or
SEVERE
CRITICAL
GCS =14
GCS = 15
No Loss of Conciousness
No Amnesia
GCS = 15 plus EITHER
Brief LOC (<5min) OR
Impaired alertness or
memory
GCS = 9-13 LOC≥ 5min Focal Neurologic Deficit
GCS = 5-8
GCS = 3-4

16. CLASSIFICATION OF TBI
• Brain injury from trauma results from two distinct processes:-
Secondary brain injury:
Develops subsequent to initial injury.
Intracranial hematoma
Edema
Hypoxemia
Ischemia (due to ICP
and/or Shock)
Vasospasm

17. INDICATIONS FOR CT AND ADMISSION CRITERIA FOR TBI
FINDINGS WITH LOW RISK OF
ICI
• Asymptomatic
• History of amnesia
• Dizziness
• Scalp hematoma, laceration,
contusion or abrasion
• NO LOSS OF CONCIOUSNESS
• CT scan is not
usually indicated.
• Plain SXRs are
not
recommended
99.6% of SXRs in
this group are
normal.
Sample discharge
instruction for head injuries
To seek medical attention for
any of the following:
• A change in level of
consciousness (including
difficulty in awakening)
• Abnormal behavior
• Increased headache
• Slurred speech
• Persistent vomiting
• Seizures
• Significant increase in
swelling at injury site.
Not to take sedatives or pain
medication stronger than
Paracetamol for 24 hrs.

18. INDICATIONS FOR CT AND ADMISSION CRITERIA FOR TBI
Findings with moderate risk
of ICI
• H/o change or loss of
consciousness
• Progressive amnesia
• Ethanol or drug intoxication
• Post-traumatic seizure
• Unreliable or inadequate
history
• Age< 2yrs
• Vomiting
• Signs of basilar skull
fracture
• Multiple trauma
• p/o skull penetration or
depressed fracture
• Suspected child abuse
Unenhanced brain
CT scan:
May miss important
lesions
(mainly hemorrhagic
contusions)
Criteria for observation at
Home
• Normal cranial CT.
• Initial GCS≥ 14
• No moderate risk criteria except
LOC
• Patient is now neurologically
intact
• There is a responsible, sober
adult that can observe the
patient
• Patient has reasonable access
to return to the hospital if
needed
• No “complicating circumstances
(e.g. suspicion of domestic
violence, child abuse)
In- hospital
observation
To rule out neurologic
deterioration if patient
doesn’t meet the criteria
or where CT scan is not
done.

19. Findings with high risk of
ICI
• Depressed level of
consciousness not clearly
due to ethanol, drugs,
metabolic abnormalities,
postictal, etc.
• Focal neurologic findings
• Decreasing level of
consciousness
• Penetrating skull injury or
depressed fracture
Management
recommendations
• Stat unenhanced brain CT
scan
• Patient is admitted
• If there are focal findings,
OT notified to be on standby
For rapid deterioration
emergency burr holes are
considered

21. INITIAL MANAGEMENT OF THE UNRESPONSIVE PATIENT
WITH BRAIN INJURY
AIRWAY/BREATHING – intubation with controlled ventilation.
Routine hyperventilation should be avoided, hyperventilation causes
vasoconstriction and can worsen cerebral ischemia.
CIRCULATION –
To restore intravascular volume, blood pressure, and perfusion.
To avoid hypotonic and dextrose containing solutions.
DISABILITY – Immobilization and serial neurologic examination
To immobilize the patient with full spine precautions and cervical spine
collar.
Documentation of GCS:
a. Intubated – e.g. GCS 11T
b. Intubated & pharmacologically paralysed – e.g. GCS 3TP

22. DRUGS :
a. Analgesia: Fentanyl or Morphine.
b. Sedation: Propofol, long acting benzodiazepines are avoided.
c. Paralytics: Vecuronium, Cisatracurium, or Succinylcholine.
MONITORING:
Continuous monitoring and recording of blood pressure and O2 saturation.
LABORATORY EVALUATION:
To check for ABGs, blood glucose, electrolytes, PT, APTT, Hct & PLT count.
With active therapy for elevated ICP, serum sodium levels and osmolality should be tracked
frequently.

23. FACTORS TO ASSESS HEAD INJURY PRIOR TO
TRANSFER
CLINICAL CONCERN ITEMS TO CHECK STEPS TO REMEDY
HYPOXIA OR
HYPOVENTILATION
ABG & Respiratory Rate To intubate any patient with hypercarbia,
hypoxemia
HYPERTENSION OR
HYPOTENSION
Blood Pressure, Hgb/Hct To transfuse patients with significant loss of
blood volume
ANEMIA Hgb/Hct To transfuse patients with significant anemia
SEIZURES Electrolytes, AED levels To correct hyponatremia or hypoglycemia,
Administration of appropriate AED.
INFECTION OR
HYPERTHERMIA
WBC, temperature LP if meningitis is possible, use of Broad-
spectrum antibiotics
SPINAL STABILITY Spine X-rays Spine immobilization (spine board, cervical
collar, etc.)

24. TREATMENT OF SEVERE TBI
A. Intensive care management of patients with severe TBI (GCS ≤ 8)
• Goal is to prevent secondary brain injury by limiting focal cerebral ischemia, preventing cerebral
hypoxia, and maintaining adequate cerebral perfusion.
1. PHYSIOLOGIC MONITORING:
a. Arterial blood pressure: NIBP can be used but an arterial catheter is preferred.
b. Heart rate, ECG, temperature & pulse oximetry
c. CVP or pulmonary artery catheter monitoring.
d. Fluid balance (Intake & output)
e. Lab evaluation:
ABGs every 4-6 hrs initially,
electrolytes, glucose, serum osmolality (if receiving mannitol) every 6 hrs.
Hgb/ Hct, PT, PTT, platelets every 12hrs.
f. ICP monitoring.

25. 2. INITIAL TREATMENT:
a. Blood pressure: MAP >80 mm Hg.
No role of anti-hypertensive before CT brain & ICP monitoring performed.
b. Oxygenation / Ventilation: to keep pO2 >60 mm Hg and pCO2 - 34-40 mm Hg. (normocapnia)
c. Volume status: CVP – 8-15 cm. of H2O and Hct ≤ 32%
d. Glycemic control / Tonicity: to avoid dextrose containing I.V solution for 1st 24 hrs.
e. Coagulation profile correction
f. Normothermia: temperature < 99ºF.
g. Anticonvulsant prophylaxis:- Phenytoin administration for 1st 7 days.
always to be administered by giving a test dose and subsequent monitoring of
myocardial depression.
h. Steroids: NO INDICATION FOR USE OF STEROIDS IN TBI.
i. Nutrition: aim – 25-30 kcal/kg/day with either enteral or parenteral supplementation.
(TBI may increase calorie requirements by 25%)

26. 3. ICP monitoring: Indications:-
 Severe closed head injury (GCS ≤ 8) and abnormal CT of head.
( hemorrhage, intracerebral hematoma, parenchymal contusion)
 Severe closed head injury (GCS ≤ 8) and normal Ct of head with two or more of the following:
• Age >40 years,
• Unilateral or bilateral flexor or extensor posturing,
• Systolic blood pressure < 90 mm Hg.

27. STEPS FOR THE MANAGEMENT OF ELEVATED ICP
HEAD OF BED
ELEVATED
Systemic
Neuromuscular
Paralysis &
Narcotic sedation
Intermittent
ventricular
CSF
drainage
Bolus Mannitol 25-50g IV/4hrly
( not used if Sr. Osm >315mOsm, or Na >150mEq/L)
Lasix
20-40mg
IV/ 4hrly
Hyperventilation
(PaCO2 – 28-30mm Hg)
Phenobarbital
(400-1000 mg IV over 1hr.)
then 40-100mg/hr.
(titrated to maintain normal
cardiac output)

28. TYPES OF HEAD INJURY
• Mainly divided into two categories:
1. Open injury:
a. Scalp injury
b. Skull fractures
2. Closed injury:
a. Concussion
b. Contusion
c. Extra-dural hemorrhage (EDH)
d. Sub-dural hemorrhage (SDH)
e. Sub-arachnoid hemorrhage (SAH)
f. Diffuse axonal injury (DAI)

29. Scalp injury
• Blunt or penetrating trauma to the head can cause injury to the densely
vascularized scalp, and significant blood loss can occur.
• Types:-
1. Caput Succedaenum
2. Cephal-Haematoma
3. Abrasion
4. Contusion (Bruise)
5. Laceration
6. Avulsion

30. CAPUT SUCCEDAENUM
• It is due to scalp edema which occurs in the newborn following trauma
during prolonged engagement of the head at the pelvic outlet.
• Presentation:
• Boggy swelling seen at birth
• Treatment:-
• usually subsides spontaneously within 2–3 days.

31. Cephal-Haematoma
• It is a subperiosteal haematoma occurring almost exclusively as a result of
birth trauma.
• Usually following forceps delivery.
• The pericranium meets the endocranium at the suture lines, this haematoma
takes the shape of the underlying bone.
• Treatment:
• usually gets absorbed within a period of 2 weeks,
• may need aspiration,
• It may occasionally calcify and may require surgical excision.

32. AIMS OF MANAGEMENT OF SCALP INJURY
• Rapid and safe coverage of underlying structures
• Minimising the risk of infection
• Transforming a dirty wound into a clean wound
• Transforming an open wound into a closed wound
• Providing a durable tissue cover
• Restoring normal contour and function
• Achieving acceptable aesthetic result.

33. CLOSED INJURIES

34. CONCUSSION
• Also known as Mild Traumatic Brain Injury (MTBI)
• Definition: Alteration of consciousness without structural damage as
a result of non-penetrating traumatic brain injury (TBI).
• Alteration in confusion may include-
• confusion,
• amnesia (the hallmarks of concussion),
• or loss of consciousness (LOC)
• CT scan is normal or significant only for mild swelling which
may represent hyperemia.
• MRI demonstrate abnormalities in 25% cases where CT is
normal.

35. CONCUSSION GRADING
GRADE CANTU system AAN system
(American Association Of Neurology)
1
(mild)
1. PTA< 30 mins.
2. no LOC
1. transient confusion
2. no LOC
3. symptoms resolve in <15 mins.
2
(moderate)
1. LOC < 5mins, or
2. PTA >30mins.
As above, but symptoms last >15 mins
(still no LOC) (PTA is common)
3
(severe)
1. LOC ≥ 5mins or
2. PTA ≥ 24 hrs.
Any LOC

36. CONTUSION (Latin contusio cerebri)
• Cerebral contusion is the most frequently encountered lesion following head
injury, occurring in 20−30% of severe head injuries.
• Contusions are wedge shaped, with the apex pointing towards the white
matter.
• In a contusion, the pia is intact and, if the pia is torn, it becomes a laceration.
Contusions can occur without laceration, but a laceration is always
associated with contusion.
• It is traumatic brain injury with CT finding that include-
Low attenuation areas representing associated edema.
High attenuation areas – hemorrhagic contusions.

38. DIFFUSE AXONAL INJURY (DAI)
• Definition: Diffuse brain injury is defined as the pathology of head injured patients
who are unconscious from the moment of impact without any evidence of space
occupying intracranial lesions on computed tomography (CT) scan or magnetic
resonance imaging (MRI).
• Pathophysiology: It is caused by angular or rotational acceleration and
deceleration inertial effects and not by contact phenomena.
• The severity of axonal damage is related to the magnitude, duration and onset rate
of the angular acceleration.

39. • CLINICAL PRESENTATION
• TDAI present in an unconscious state from the onset of trauma,
• DAI are less likely to have a lucid interval.
• The chance that a patient will remain in a persistent vegetative state is greater
when lesions are observed in the supra-tentorial white matter, corpus
callosum and corona radiata.
• DAI lesions can result in deficits in information transfer between the two
hemispheres through the corpus callosum, commonly resulting in auditory
deficits.

40. CT findings in DAI
• One or more small intraparenchymal haemorrhages less than 2 cm in
diameter, located in the cerebral hemispheres
• Intraventricular haemorrhage
• Haemorrhage in the corpus callosum
• Small focal areas of haemorrhage less than 2 cm in diameter, adjacent to
the third ventricle
• Brainstem haemorrhage.

42. EXTRA-DURAL HEMORRHAGE
• Comprises of 1% of all head injury.
• Source of bleeding:
• Middle meningeal artery (85%)
• Disruption of middle meningeal veins & dural sinuses
• Sites:
• Temporoparietal (m/c)
• Frontal, occipital and posterior fossa
• Presentation
• brief post-traumatic loss of consciousness
• followed by a "lucid interval" for several hours
• obtundation, contralateral hemiparesis, ipsilateral pupillary dilatation
• In pediatric age group, EDH should be suspected if there is a 10% drop in hematocrit after
admission.

43. • Pathophysiology: Shift of the brain stem away from the mass
may produce compression of the opposite cerebral
peduncle on tentorial notch
produce ipsilateral hemiparesis (so called Kernohan's
phenomenon), a false localizing sign.

44. KERNOHAN’S PHENOMENON

45. SUBDURAL HEMATOMA
 Collection of blood in the
subdural space.
Due to tear of bridging veins.
Acute SDH: 1—3 Days
Sub-acute SDH: 4 days to
2 or 3 wks
Chronic SDH: > 3 wks

46. ACUTE SUBDURAL HEMATOMA
 Traumatic in origin
 Incidence: 50% of HI at
casualty.
Magnitude of impact is
much higher.
Hematoma is extensive
& diffuse.

47. Accumulation around
parenchymal injury.
 Associated severe
underlying primary brain
injury.
 No lucid interval
 Focal signs occur later
& less prominent.
 Cerebral acceleration-
decceleration during violent
head motion.
 Tear of bridging veins.
 No or less primary brain
damage.
 Lucid interval may
occur.
TWO COMMON CAUSES OF TRAUMATIC SDH

48. PRESENTATIONS
Features Acute EDH Acute SDH
Loss of consciousness Early/Late
Transient
Early
Persistent
Lucid interval Present(6-12hrs) Absent or <1hr
Raised ICP ++, Late +++, early
Neurological deficit ++ +++
Herniation Late Early
Kernohan’s
phenomenum
+++ +++
Seizures + ++

49. EVALUATION BY CT SCAN
Acute EDH
 Classical CT
appearance:
 High density
biconvex(lenticular)
shape.
Mass effect with midline
shift

50. Acute SDH
Hyper-dense crescentic
mass adjacent to inner
table.
Associated cerebral
edema.
Location:
Lateral hemispheric
convexity
Inter-hemispheric
Posterior fossa

51. SDH density changes with time
Category Time frame Density on CT
Acute 1 to 3 days Hyperdense
Sub-acute 4 days to 2—3 wks Isodense
Chronic > 3 wks and < 3 months Hypodense

53. Treatment of Acute EDH/SDH

54. Acute EDH
 Immediate evacuation by craniotomy.
 Indications:
Any symptomatic EDH or GCS<8
An asymptomatic EDH>1cm in its thickness
Midline shift>5mm
EDH in pediatric patients.

56. ACUTE SDH
 Rapid surgical evacuation & hemostasis by large craniotomy.
Indicated in:
symptomatic SDH that are >1cm thick.
Midline shift>5mm
Drop of GCS>2

58. Outcome of surgery in Acute SDH
Depends on
 Age
 Time to surgery( Four hour rule)
 30% mortality if operated <4hrs
90% mortality if operated >4hrs
 Post operative ICP
Admission GCS
GCS Mortality Functional survival
3 90% 5%
4 76% 10%
5 62% 18%
6 -- 7 51% 44%

59. ROLE OF MEDICAL MANAGEMENT
Indicated if size<1cm & asymptomatic.
Management includes:
 Close observation
Steroids & antiepileptics
Follow up CT ( in 1 wk & then 1—3 month if clinically stable)
Urgent CT & surgery if signs of mass effect/signs of herniation)

60. MORTALITY
Acute SDH
• Range: 50-90%
• Usually due to underlying brain
injury.
• Higher in aged.
Acute EDH
•Range 2-18%
•Usually due to
secondary brain injury

61. CHRONIC SUBDURAL HEMATOMA
• Usually occur in elderly people(>60yrs).
• Risk factors:
 H/O head injury(<50%), often trivial.
Alcoholic
Seizures
Coagulopathies
• Bilateral in 25% cases.

62. PATHOPHYSIOLOGY including sequalae
Starts as acute SDH.
Ingrowths of neomembranes, neocapillaries, enzymatic fibrinolysis
and liquefaction of blood clot.
Chronic subdural effusion or Re-bleeding
(Volume expansion)
Infection leading to subdural empyma

63. PRESENTATIONS
 Minor symptoms:
 Headache, confusion, disorientation.
 Gradual altered level of consciousness.
Major symptoms
 Features of raised ICP
 Seizures
 Hemiplegia
 Coma

64. CT diagnosis

65. TREATMENT
 Seizure prophylaxis by AEDs
Treat any coagulopathy
Surgical evacuation of hematoma if
 Symptomatic lesions
Size>1cm in thickness
Midline shift>5mm
Sudden drop of GCS >2

66. SURGICAL OPTIONS
1) Burr hole drainage
 Single large burr hole with
irrigation and aspiration
 Single burr hole with subdural
drain placement
 Two burr holes with irrigation
2) Twist drill craniostomy
3) Craniotomy & evacuation

67. Twist drill craniostomy

69. COMPLICATIONS OF SURGERY
Seizures
Intracerebral hemorrhage:
In 0.7-5%
Recurrence i.e., reaccumulation
Tension pneumocephalus
Subdural empyema
Overall mortality following surgery 0-8%.

70. SUB-ARACHNOID HEMORRHAGE

71. INTRODUCTION
• Bleeding into the subarachnoid
space surrounding the brain.
• SAH is a form of stroke and
comprises 1–7% of all strokes.
• Up to half of all cases of SAH are
fatal and 10–15% of casualties die
before reaching a hospital

72. ETIOLOGY
Traumatic –
bleeding from 3 sources:
• Direct injury to pia vessels
• Hemorrhagic cortical contusion
(IPH)
• Extension from intraventricular
hemorrhage
Non-traumatic (less
common):
– Ruptured aneurysms (75%) --
Occur at branching points of
circle of Willis
– Ruptured AVMs (10%)
– Uncommon causes
neoplasms, dural AVM, venous
angiomas, infectious
aneurysms

73. ANEURYSMS
1-2% of the population have
unruptured aneurysms
 Any aneurysm can rupture, larger
(>1cm ) aneurysms r more likely to
do so.
 Women > Men, incidence
increases linearly with age
 10-15% of patients presenting with
SAH have multiple aneurysms

74. SITES of brain aneurysm
Prevalence Aneurysm location
Anterior
circulation(95%)
Anterior communicating artery-36%
Posterior communicating artery-21%
Middle cerebral artery-38%
Posterior
circulation(5%)
Posterior inferior cerebellar artery-5%

75. PRESENTATION
“Thunderclap”: headache:
Abrupt, maximum at onset
Worst headache in life.
First headache ever of this type & intensity
Vomiting
Loss of consciousness
Diplopia
Nuchal rigidity
Seizure
Focal neurological deficit

76. DIAGNOSIS
1) CT scan(plain):
The initial study of choice.
 90% sensitive within the 1st 24 hrs, 80%
sensitive at 3 days, and 50% sensitive at 1
week.
 Detect ICH,mass effect, and hydrocephalus.
Trauma high attenuation in sulci.
 Aneurysm high attenuation in basilar
cisterns (region of circle of Willis-- “star”
pattern )

77. 2) MRI:
More sensitive than CT after several
days.
Detects structural causes like AVMs.
3) Angiography:
 Cerebral angiography
 MR more sensitive than CT angio.
 Delineates
 Location of ruptured aneurysm
 Size of unruptered aneurysms.
 Visualize "Neck“

78. 4) Lumbar puncture:
 mandatory in suspected SAH if imaging
is negative.
 3 tubes of CSF are collected, elevated
number of red blood cells is present
equally in all bottles.
 xanthochromia—the yellow
appearance of centrifugated fluid.
 spectrophotometry for detection
of bilirubin.

79. COMPLICATIONS
1) Rebleeding:
• 20% of patients in the first 2 weeks.
• Peak incidence within 24 hrs.
• This may be from lysis of the aneurysmal clot.
2) Arterial vasospasm:
• In 35% of patients within 4-14days
• Cause infarct.
3) Hydrocephalus:
• Within the first 24 hours because of obstruction of CSF outflow
in the ventricular system by clotted blood.

80. 4) Neurologic deficits:
• Peak at 4-14days due to cerebral ischemia
5) Hypothalamic dysfunction:
• Excessive sympathetic stimulation.
• lead to MI or hypertension.
6) Hyponatremia/SIADH
7) Seizures.

81. TREATMENT
AIMS:
 Initial stabilization
Identifying and treating the causative lesion, thus
preventing rebleeding
Treating hydrocephalus if any
Treatment & prevention of vasospasm.

82. PREVENT REBLEEDING
 Cerebral angiography to detect ruptured
aneurysm.
 Early aneurysmal occlusion(<3days or >10days)
Two options of occlusion:
Craniotomy & clip application
Endovascular coil placement.

83. CLIP APPLICATION
INDICATIONS:
• Young age
• Good medical condition
• Broad aneurysm neck
COIL PLACEMENT
INDICATIONS:
• Old age
• Co morbidity
• Narrow aneurysm neck.

84. PREVENT VASOSPASM
Use calcium channel blocker like Nimodipine.
HHH therapy
 Hypertension( Target BP:140/90)
 Hypervolemia( Normal saline+albumin)
 Hemodilution( Hct<33%)
Endovascular balloon angioplasty

85. PROGNOSIS
Disease of poor outcome.
Mortality for SAH is between 40 and 50% in 30days.
High residual disability & long term sequele in 2/3rd survivors.

86. COMPLICATIONS FROM TRAUMATIC
BRAIN INJURY
1. Posttraumatic seizures
2. Communicating hydrocephalus
3. Posttraumatic syndrome (or post-concussive syndrome)
4. Hypogonadotropic hypogonadism
5. Chronic traumatic encephalopathy
6. Alzheimer's disease (AD)

87. CONCLUSION
• Morbidity & mortality is high in any type of intracranial
hemorrhage.
• More if primary treatment is delayed.
• Critical care to assess and resuscitate to prevent secondary
brain injury,
• Early identification of intracranial pathology that can be
treated by surgery.
• Preventing complications that reduce the chances of best
possible recovery.