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1. Management of Traumatic
Brain Injury
Dr.ehsan ziaeii (neurosurgeon)

2. Traumatic brain injury (TBl) constitutes a critical public health
and socioeconomic problem throughout the world. It is the
leading cause of mortality and disability among young individuals
the incidence of TBI is rising sharply, mainly because of increasing
motor vehicle use

3. Level Of Consciousness
• Glasgow Coma Scale
Eye Opening Best Verbal Best Motor
Spontaneous 4 Oriented 5 Obeys Command
6
To Voice 3 Confused 4 Localizes 5
To Pain 2 Inappropriate 3 Withdraws 4
None 1 Incomprehensible 2 Flexion 3
None 1 Extension 2
None 1

6. CONCUSSION
Definition: Alteration of consciousness with out structural damage as a
result of nonpenetrating traumatic brain injury (TBI).
Alterations in consciousness may include: confusion, amnesia (the
hallmarks of concussion),or loss of consciousness (LOC). Loss of
consciousness is not a requirement

7. CONCUSSION
There are no gross or microscopic parenchymal
abnormalities. CT is normal or significant only for
mild swelling which may represent hyperemia

8. CONCUSSION

9. Criteria for observation at home
1. normal cranial CT
2. initial GCS>14
3. No high risk criteria
4. patient is now neurologically intact
(amnesia for the event is acceptable)
6. there is a responsible
7. Patient has reasonable access to return to the hospital if needed
8. no "complicating" circumstances (e.g.no suspicion of domestic
violence, including child abuse

10. High risk
:
1.a change in level of consciousness (including
difficulty in awakening)
2.abnormal behavior
3.increased headache
4.slurred speech
5.weakness or loss of feeling in an arm or leg
6.persistent vomiting
7.enlargement of one or both pupils
8.seizures (convulsions or fits)
9.significant increase in swelling at injury site
10.Neurologic defecit

11. ADMITTING ORDERS FOR MINOR OR MODERATE
HEAD INJURY
1. activity: BR with HOB elevated 30-45.
2. neuro checks q 2 hrs .Contact physician for neurologic deterioration
3. NPO until alert; then clear liquids, advance as tolerated
4. isotonic IVF (e.g. NS + 20 mEq KCI/L)
5. mild analgesics: acetaminophen (PO. or PR ifNPO). codeine if
necessary
6. anti-emetic

12. Admitting orders for moderate head injury
(GCS 9-13)
1. orders as for minor head injury except patient is kept NPO in case
surgical intervention is needed (including lCP monitor)
2. for GCS = 9-12 admit to lCU. For GCS =13. admit to lCU if CT shows
any significant abnormality (hemorrhagic contusions unless very small,
rim subdural.)
3. patients with normal or near-normal CTs should improve within
hours. Any patient who fails to reach a GCS of 14-15 within 12 hrs
should have a repeat CT at that time

14. Secondary Brain Injury
Biochemical Cascade Blood Flow
changes(Global/regional)
External Compression
AA/Neurotransmitter
release
Uncoupling of Substrate
delivery and extraction
Intraparenchymal
Extraxial
(subdural/epidural)
Intracellular Ca++
accumulation and
cytoskeletal/ enzymatic
breakdown
Pneumocephalus
Depressed skull fracture
Extracellular Cytokines and
GF
Generation of free radicals
CMRoxy
CMRglucose
CBF OEF/GEF

15. hypoxia
Hypoxemia is also one of five powerful indictors of patient
outcome after TBi Severe oxygen desaturation «60%) during
transport to tile hospital is associated with a 3.5-fold increase in
mortality

16. hypoxia
in acute injury phase, hypoxia is typically due to severe
hypoventilation,airway obstruction, aspiration, or hemothorax and
pneumothorax.
On the other hand, in the first 24 to 48 hours after TBl,most
episodes result from lung contusions, atelectasis, fat emboli,
pneumonia, or acute lung disease.

17. Systemic Hypotension
Hypotension is one of the five most powerful indicators of
outcome after TBI and strongly correlates with poor neurological
recovelyY04, A single episode of hypotension after
TBI increases morbidity and doubles mortality,2 whereas two or
more episodes increase the relative risk for mortality to 8.1.

18. Hyperthermia
.
For each degree Celsius elevation in body temperature,
cerebral metabolism increases by 10% to 13%
fever leads to increased CBV with resultant elevation of ICP and
reduction of CPP

19. pain
pain after TBI is a significant source of secondaly
injury tlhat is strongly associated With worse neurological
Outcome.

20. PRACTICE GUIDELINE
leuel II": monitor BP and avoid hypotension (SBP < 90
mm Hg)
leuel III": monitor oxygenation and avoid hypoxia
(Pa02 < 60 mm Hg or O2saturation < 90%)

21. Leuelll: secure the airway (usually by endotracheal intubation) in patients
with GCS <8 who are unable to maintain their airway or who remain hypoxic
despite supplemental O2Cautions regarding intubation:
1. if basal skull fracture through cribriform plate is possible, avoid
nasotracheal intubation(to avoid intracranial entry of tube). Use orotracheal
intubation
2. prevents assessment of patient's ability to verbalize e.g. for determining
Glasgow Coma Scale score
3. risk of pneumonia:

22. •prophylactic hyperventilation (PaC02 s 25 mm
Hg) is not recommended

23. prophylactic phenytoin, carbamazepine, phenobarbital or Valproate do
not prevent late PTS
AEDs" (e.g. phenytoin, valproate, or carbamazepine) may be
used to decrease the incidence of early PTS (within 7 days ofTB) in
patients

24. Conditions with increased risk of posttraumatic
seizures
1. acute subdural,epidural,or intracerebral hematoma
2. open-depressed skull fracture with parenchymal injury
3. seizure within the first 24 hrs after injury
4. Glasgow Coma Scale score < 10
5. penetrating brain injury
6. history of significant alcohol abuse
7. cortical contusion on CT

25. Skull Fractures
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),

26. “Ping-pong” fractures are greenstick-type fractures
usually seen in newborns due to the plasticity of the
skull . They show a local concavity of the skull, without
sharp edges, and usually do not require intervention

29. • Cerebral Contusion
Cerebral contusions are injuries to the superficial gray matter of
the brain caused by a focal force
On CT scans, contusions are patchy, hyperdense lesions
with a hypodense background. Contusions may
coalesce or enlarge within the first 12 hours and the associated
edema will often worsen over the first several days. Vigilant
monitoring of the patient with a contusion is essential, and
repeat CT scanning is frequently required.

30. Epidural Hemorrhage
EDH occurs when blood collects in the potential space between
the dura and inner table of the skull. It is seen in 1% of all
head trauma admissions and in 5–15% of patients with fatal
head injuries. It is more common in males (M:F ! 4:1), usually
occurs in young adults, and is rarely seen in ages #2 or "60
since the dura is more adherent to the inner table of the skull
in these groups.

31. On CT scan, EDHs usually appear as a hyperdense,
biconvex (lenticular) mass adjacent to the inner
table of the skull

34. Rapid diagnosis and intervention when indicated is paramount
to optimize the outcome. Surgical guidelines suggest
that EDH of >30 cc should be evacuated regardless of GCS
score. EDH of <30 and <15 mm of thickness and
<5 mm midline shift may be treated conservatively at a neurosurgical
center with frequent neurological examinations and
serial CT scanning. Relative indications exist for resection of
EDHs that are neurologically symptomatic or have a maximal
thickness >1 cm. Patients with acute EDH in coma (GCS <8)
and anisocoria should undergo surgical evacuation as soon as
possible

35. Subdural Hemorrhage
SDH occurs when blood collects between the arachnoid and
inner dural layer and is usually divided into hyperacute
(#6 hours), acute (6 hours to 3 days), subacute (3 days to
2 weeks), and chronic (2 weeks to 3 months) variants

38. SDHs are commonly located over the hemispheric convexities
and may cover part or all of a hemisphere (holoconvexity
SDH). Classically, they are crescent shaped, cross suture
lines, and layer along the falx or tentorium

39. Guidelines suggest that an acute SDH with thickness
>1 cm or a midline shift >5 mm should be evacuated regardless
of GCS score. Patients with acute SDH <1 cm thick and
midline shift <5 mm and in coma (GCS <8) should undergo
SDH evacuation if the GCS decreases by 2 points between the
time of injury and hospital admission, if they present with
pupils that are asymmetric or fixed/dilated, or if the ICP
>20 mm Hg

40. Intraparenchymal Hemorrhage
IPH or traumatic intracerebral hemorrhage (TICH) is seen
in up to 8.2% of all TBI and up to 35% of severe TBI cases.
Similar to contusions, TICH and associated edema may increase over
time and produce increasing mass effect and neurological
deterioration. Delayed traumatic intracerebral hemorrhage (DTICH) will
appear in approximately 20% of cases and most occur within 72 hours
of the initial trauma

41. ICH
If patients develop neurological decline referable to the
TICH lesion such as IC-HTN refractory to medical treatment
or increasing mass effect with impending herniation, surgical
decompression is warranted. Investigation of patient subtypes
has shown that surgical decompression is often necessary in
patients with TICH >50 cm 3 , or patients with GCS > 6–8 who
have frontal or temporal contusions >20 cm 3 with midline
Shift >5 mm and/or cisternal compression on CT scan.

42. Hyperosmolar Therapy
While the exact mechanism by which mannitol provides beneficial
outcome is unclear, two primary methods are postulated.
In the first few minutes, it produces immediate plasma expansion
with reduced hematocrit and blood viscosity, improved
rheology, and increased CBF and O 2 delivery. This reduces ICP
and is most notable in patients with CPP <70 mm Hg.
Over the next 15–30 minutes, and lasting 1.5–6 hours, mannitol
produces an osmotic effect with increased serum tonicity
and withdrawal of edema fluid from the cerebral parenchyma

43. When given as a bolus, the ICP reduction is evident at
1–5 minutes and peaks at 20–60 minutes. The initial bolus of
mannitol, for acute ICP reduction in cases of neurological
worsening or herniation, should be dosed at 1 g/kg with subsequent
administration at smaller doses and longer intervals (i.e.,
0.25–0.5 g/kg Q 6 hours). Mannitol opens the blood–brain
barrier (BBB) and may cross the BBB itself, drawing water into
the brain and transiently exacerbating vasogenic cerebral
edema

44. Hypertonic Saline
As with mannitol, hypertonic saline (HS) is thought to lower
ICP through two mechanisms. First, an oncotic pressure gradient,
across the BBB, results in mobilization of water from brain
tissue and hypernatremia. Second, rapid plasma dilution and
volume expansion, endothelial cell and erythrocyte dehydration,
and increased erythrocyte deformability lead to improvements
in rheology, CBF, and oxygen delivery.

45. Steroids
Glucocorticoids are not recommended for improving outcome
or reducing ICP in Side effects of steroid use include
coagulopathies, hyperglycemia, and increased infection and
are reflected in poor outcomes

46. POST TRAUMATIC SEIZURES
1. Early posttraumatic seizures within min
to hours of injury.
1. No radiological intracranial injury
noted in many cases
2. Do not portend later epilepsy
3. Most do not need Rx
4. Outcome good.
• Late seizure  >24 hrs after
injury
– Visible intracranial injury.
– Penetrating injuries/
depressed #/ SDH/ Lower
GCS score
– Long term risk of epilespy
high- need Rx for 6-12 mo.
• Seizure prophylaxis
Only during first week Or till
intracranial hypertension
phase is passed.
Prolonged usage has
cognitive deficits on long
term follow ups.
Phenytoin commonly used