This document provides an overview of traumatic brain injury (TBI). It defines TBI and discusses its epidemiology. It then covers the pathophysiology of TBI, including primary and secondary brain injuries. It also classifies TBI based on clinical examination and imaging findings. The document outlines recommendations for monitoring TBI patients and discusses common complications. Finally, it summarizes guidelines for managing severe TBI, including treatments aimed at reducing intracranial pressure and optimizing cerebral perfusion.

1. Traumatic
Brain Injury
Mohammed Abdelmon`em El Besh
M.B.B.CH (2010)

2. Highlights
• Definition
• Epidemiology
• Pathophysiology
• Classification
• Monitoring
• Complication
• Management and recommendations

3. Definition
• Traumatic brain injury (TBI) is a
nondegenerative, noncongenital insult to the
brain from an external mechanical force,
possibly leading to permanent or temporary
impairment of cognitive, physical, and
psychosocial functions, with an associated
diminished or altered state of consciousness.

4. Epidemiology
• Traumatic brain injury (TBI) is a contributing
factor to approximately one-third of all injury-
related deaths in the USA annually.
• Updated statistical records for TBI in Egypt
are lacking.

5. Age (years) NO = 844/
4 months
FFH MVC Abuse/
neglect
Violence/
assaults
Struck by/
against
Other
causes/ not
known
1 to 5 54 (6%) 20 (37%) 10 (19%) 8 (15%) - 8 (15%) 8 (14%)
6 to 18 91 (11%) 28 (31%) 20 (22%) 5 (6%) 6 (5 %) 22 (25%) 10 (11%)
19 to 29 150 (18%) 49 (33%) 45 (30%) - 14 (9%) 18 (12%) 24 (16%)
30 to 55 381 (45%) 114 (30%) 134 (35%) - 19 (5%) 50 (13%) 64 (17%)
Above 55 168 (20%) 47 (28%) 41 (24%) 11 (7%) 5 (3%) 25 (15%) 39 (23%)

6. Pathophysiology
Altered cerebral auto regulation
brain’s mechanism of maintaining adequate and
stable blood flow despite changes in perfusion pressure.
Primary injury:
which occurs at the moment of trauma
Secondary injury
which occurs immediately after trauma and produces effects
that may continue for a long time.

7. Pathophysiology: Altered Cerebral Auto-regulation
• Cerebral blood flow is maintained over a range of a cerebral perfusion pressure of
60 to 160 mm Hg (cerebral perfusion pressure is the total of intracranial pressure
[ICP] subtracted from MAP).
• Above and below this range, CA is lost, and blood flow depends on MAP in a
linear fashion In this setting, if cerebral blood flow decreases because of
hypotension, compensation includes increased oxygen extraction.
• Once this compensatory mechanism is exhausted, cerebral ischemia and
infarction can occur. Alternatively, if cerebral blood flow increases because of
hypertension, vascular constriction is overcome by excessive intravascular
pressure. This increased pressure experienced by the cerebral endothelium may
lead to edema formation and eventual herniation.

8. Pathophysiology: Primary Brain injuries
• Primary injury refers to initial damage occurring at the moment of impact, which
involves mechanical forces that shear and compress neurons, glia, and vascular
tissue. This initial damage leads to physical disruption of cell membranes and
their infrastructure with subsequent increase in membrane permeability and
disturbance of ionic homeostasis. This initial damage in turn leads to cellular
swelling, relative hypoperfusion, and a cascade of neurotoxic events
• Primary injuries can manifest as focal injuries (eg, skull fractures, intracranial
hematomas, lacerations, contusions, penetrating wounds), or they can be diffuse
(as in diffuse axonal injury).

9. Pathophysiology:
Secondary Brain injuries
• Secondary types of traumatic brain injury (TBI) are attributable to further
cellular damage from the effects of primary injuries. Secondary injuries may
develop over a period of hours or days following the initial traumatic assault
• Excitatory amino acids (EAAs), including glutamate and aspartate, are
significantly elevated after a TBI. EAAs can cause cell swelling, vacuolization,
and neuronal death.
• Endogenous opioid peptides : These may contribute to the exacerbation of
neurologic damage by modulating the presynaptic release of EAA
neurotransmitters.
• Increased intracranial pressure (ICP):The severity of a TBI tends to increase due
to heightened ICP, especially if the pressure exceeds 40 mm Hg. Increased
pressure also can lead to cerebral hypoxia, cerebral ischemia, cerebral edema,
hydrocephalus, and brain herniation.

10. • Cerebral edema:Edema may be caused by the effects of the above-
mentioned neurochemical transmitters and by increased ICP. Disruption
of the blood-brain barrier, with impairment of vasomotor autoregulation
leading to dilatation of cerebral blood vessels, also contributes.
• Hydrocephalus :The communicating type of hydrocephalus is more
common in TBI than is the noncommunicating type
• Brain herniation: Supratentorial herniation is attributable to direct
mechanical compression by an accumulating mass or to increased
intracranial pressure

11. CLASSIFICATION
Head Injury Classification Based on Clinical
Examination
• Glasgow Coma Scale
• Duration of loss of consciousness
• Posttraumatic amnesia (PTA)
Head Injury Classification Based on Imaging
• Marshall Classification

12. CLASSIFICATION:
Glasgow Coma Scale

13. Classification
Based on Imaging
• Marshall Classification: The grading system applies to CT scans
performed in patients with nonfocal injury and accounts for the status of
the mesencephalic cisterns, the degree of midline shift in millimeters,
and the presence or absence of 1 or more surgical masses

15. Limitation of Marchell classification
• Lack of tSAH
• Basis of volume of mass lesion as 25 cc is not clear
• Does not classify type of hematoma
• Does not further categorize extent of basal cisterns
compression
• Cannot be used as grading system
• Rotterdam CT grading overcomes limitations

16. Rotterdam Grading of CT Scan

17. Monitoring
• The core physiological monitor used in TBI is ICP monitoring and
Haemodynamics , in addition to standard monitoring used for any
critically ill patient
• The oxygen saturation level and the PCO2 level
• coagulopathy.
• serum Na determinations, urine output
• Other TBI-specific physiological monitors are less widely used
– SjO2:
• Jugular venous bulb oximetry involves placing a sampling catheter in the internal jugular vein,
directed upwards, so that its tip rests in the jugular venous bulb at the base of the brain
• This is normally in the range 50-75%.
• The SjO2 will fall when there is an imbalance between oxygen consumption and delivery

18. • Microdialysis: a laboratory tool that provides on-line analysis of brain
biochemistry (Like lactate, excitatory amino acids, glycerol, glucose, and
pyruvate as well as other metabolic compounds during periods of metabolic
stress of TBI) via a thin, fenestrated, double-lumen dialysis catheter that is
inserted into the interstitium of the brain.
• Ocular ultrasound for optic nerve sheath diameter
• Brain tissue oxygen (PbtO2) monitoring. The investigators showed that a
protocol designed to maintain PbtO2 at more than 20 mm Hg effectively reduced
the duration of brain tissue hypoxia

19. UpdatedMonitoring
Recommendations TBF 2017

20. Updated Recommendations: Thresholds

21. Complications
• The primary complication of TBI i s secondary brain injury that can
compound the neurologic morbidity and mortality. The most severe
result is progression to herniation and brain death.
• Systemic Complications :
– Seizures-can occur early (first 7 days) or late.
– Coagulopathy-release of tissue factors may result in increased fibrinolysis and
hypocoagulable state. This may progress to disseminated intravascular coagulation
(DIC) .
– Cardiopulmonary complications-myocardial infarction, cardiomyopathy,ARDS, and
heart failure.
– Deep venous thrombosis and pulmonary embolus-
– Infection-patients with head injuries are at risk for ventilator-related pneumonia, line
sepsis, and other infections. CSF leaks increase risk for meningitis.

22. – Diabetes insipidus
– Syndrome of inappropriate antidiuretic hormone (SIADH)-
– Cerebral salt wasting-poorly understood condition where volume and sodium are
excreted in the urine, resulting in hypovolemia and hyponatremia.

23. Management :
Guidelines for the Management of Severe Traumatic
Brain Injury, Fourth Edition 2017
• The overarching goal of treatment in patients with TBI is to minimize the
progression of secondary brain injury, namely ischemia, by reducing
cerebral edema and ICP while maintaining cerebral perfusion, oxygen
delivery, and energy to the brain.
• Simply put, the goal is to squeeze oxygenated blood through a swollen
brain
• SEVERE TRAUMATIC BRAIN INJURY (GCS 3-8)
• Management recommendation is based on Guidelines for the
Management of Severe Traumatic Brain Injury, Fourth Edition 2017

24. BTF TBI 2017 : level of evidence
• The levels were primarily based on the quality of the body of evidence as
follows:
• Level I recommendations were based on a high-quality body of
evidence.
• Level IIA recommendations were based on a moderate-quality body of
evidence.
• Level IIB and III recommendations were based on a low-quality body of
evidence.

26. BTF TBI 2017: Topics recommendations
• Resuscitation of Blood Pressure
• ICP Treatment Algorithm
• Cerebrospinal fluid drainage
• Hyperventilation
• Osmotherapy Mannitol
• Anesthetics, analgesics, and sedatives Barbiturates
• Antiseizure Prophalyxis
• Decompressive craniotomy
• Infection prophylaxis
• Prophylactic hypothermia
• Steroids
• Nutrition

27. BTF TBI 2017:BP resuscitations
Hypotension (SBP < 90 mm Hg) or hypoxia (apnea of cyanosis in the field or a
PaO2 < 60 mm Hg) must be scrupulously avoided, if possible, or
corrected immediately.
Maintaining SBP at ≥100mmHg for patients 50 to 69 years old or at ≥110mmHg or
above for patients 15 to 49 or >70 years old may be considered to decrease
mortality and improve outcomes.
Level III

28. BTF TBI 2017:ICP Treatment
• Intracranial hypertension, which is defined as an ICP greater than 20
mm Hg for longer than 5 minutes. In approximately half of those who die
after severe TBI,

29. BTF TBI 2017:Indications for ICP Monitoring
• Management of severe TBI patients using information from ICP monitoring is
recommended to reduce in-hospital and 2-week post-injury mortality.
• ICP should be monitored in all salvageable patients with a TBI (GCS 3-8 after
resuscitation) and an abnormal CT scan. An abnormal CT scan of the head is
one that reveals hematomas, contusions, swelling, herniation, or compressed
basal cisterns.
• ICP monitoring is indicated in patients with severe TBI with a normal CT scan if
≥2 of the following features are noted at admission: age >40 years, unilateral or
bilateral motor posturing, or SBP <90 mm Hg.
Level IIB

30. BTF TBI 2017: Cerebral perfusion pressure
monitoring
Management of severe TBI patients using guidelines-based
recommendations for CPP monitoring is recommended to decrease 2-
wkmortality.
Level IIB
• Treating ICP >22mmHg is recommended because values above this level
are associated with increased mortality.
Level IIB
• A combination of ICP values and clinical and brain CT findings may be
used to make management decisions.
Level III

31. BTF TBI 2017:Cerebral perfusion pressure
thresholds
• The recommended target CPP value for survival and favorable outcomes is
between 60 and 70mm Hg. Whether 60 or 70mmHg is optimal CPP
threshold is unclear and may depend upon the autoregulatory status of the
patient.
Level IIB
• Avoiding aggressive attempts to maintain CPP >70 mm Hg with fluids and
pressors may be considered because of the risk of adult respiratory failure.
Level III

32. BTF TBI 2017: Advanced cerebral monitoring
thresholds
Jugular venous saturation of <50% may be a threshold to avoid in order to
reduce mortality and improve outcomes.
Level III

33. BTF TBI 2017:ICP Monitoring Technology
In the current state of technology, the ventricular catheter connected to an
external strain gauge is the most accurate, low cost, and reliable method of
monitoring ICP. It also allows therapeutic CSF drainage.
• ICP transduction via fiberoptic or strain gauge devices placed in ventricular
catheters provide similar benefits but at a higher cost. Cerebrospinal fluid
drainage
• • An EVD system zeroed at the midbrain with continuous drainage of CSF may
be considered to lower ICP burden more effectively than intermittent use.
• • Use of CSF drainage to lower ICP in patients with an initial GCS <6 during
the first 12 h after injury may be considered.
• Level III

34. BTF TBI 2017: Ventilation therapies
• Prolonged prophylactic hyperventilation with PaCO2 of ≤25 mm Hg is
not recommended.
• Hyperventilation is recommended as a temporizing measure for the
reduction of elevated ICP.
• Hyperventilation should be avoided during the first 24 h after injury
when CBF often is reduced critically.
• If hyperventilation is used, SjO2 or BtpO2 measurements are
recommended to monitor oxygen delivery.
Level IIB

35. BTF TBI 2017:Osmotherapy
• Hypertonic saline and mannitol are the most commonly used agents and
both are effective in reducing ICP. Both work presumably by
establishing an osmotic gradient between the brain and cerebral
vasculature, which results in a net water loss in brain tissue. Thus, in
order to effectively achieve a gradient, the blood-brain barrier must be
intact.
• The superiority of one particular agent continues to be debated,
although until recently mannitol was considered the gold standard.
• Hyperosmolar therapy Recommendations from the prior (Third) Edition
not supported by evidence meeting current standards.

36. BTF TBI 2017:Osmotherapy
• Mannitol is effective for control of raised ICP at doses of
0.25 to 1 g/kg body weight. Arterial hypotension (systolic
blood pressure <90 mm Hg) should be avoided.
• Restrict mannitol use prior to ICP monitoring to patients
with signs of transtentorial herniation or progressive
neurologic deterioration not attributable to extracranial
causes.

37. BTF TBI 2017:Hypothermia
• Cooling reduces Cerebral metabolic rate 6 % for each 1 C and so
decreases ICP
• Early (within 2.5 h), short-term (48 h post-injury), prophylactic
hypothermia is not recommended to improve outcomes in patients with
diffuse injury.
Level IIB

38. BTF TBI 2017:Anesthetics, analgesics, and
sedatives
Thiopental coma decreases metabolic requirement by 50 % and associated by
cerebral vasoconstriction and decrease of ICP
Administration of barbiturates to induce burst suppression measured by EEG as
prophylaxis against the development of intracranial hypertension is not
recommended.
High-dose barbiturate administration is recommended to control elevated ICP
refractory to maximum standard medical and surgical treatment. Hemodynamic
stability is essential before and during barbiturate therapy.
Although propofol is recommended for the control of ICP, it is not recommended
for improvement in mortality or 6-month outcomes. Caution is required as high-
dose propofol can produce significant morbidity.
Level IIB

39. BTF TBI 2017: Decompressive craniectomy
which is substantial portion of the cranium is removed and the dura opened to
increase the volume of the cranial cavity and, thus, decrease the ICP.
• Bifrontal DC is not recommended to improve outcomes as measured by the GOS-
E score at 6 mo post-injury in severe TBI patients with diffuse injury (without mass
lesions), and with ICP elevation to values >20mm Hg for more than 15min within a
1-h period that are refractory to first-tier therapies. However, this procedure has
been demonstrated to reduce ICP and to minimize days in the ICU.
• A large fronto-temporoparietal DC (not less than 12 x 15 cm or 15 cm diameter) is
recommended over a small fronto-temporoparietal DC for reduced mortality and
improved neurologic outcomes in patients with severe TBI.
Level IIA

40. Critical Pathway for Treatment of Intracranial Hypertension in the Severe
Head Injury Patient (Treatment Option)

42. BTF TBI 2017:Steroids
The use of steroids is not recommended for improving
outcome or reducing ICP. In patients with severe TBI,
high-dose methylprednisolone was associated with
increased mortality and is contraindicated.
Level I

43. BTF TBI 2017:Nutrition
Feeding patients to attain basal caloric replacement at least by
the fifth day and at most by the seventh day
post-injury is recommended to decrease mortality.
Level IIB
Trans-gastric jejunal feeding is recommended to reduce the
incidence of ventilator-associated pneumonia.
Level IIA

44. BTF TBI 2017: Infection prophylaxis
• Early tracheostomy is recommended to reduce mechanical ventilation
days when the overall benefit is thought to outweigh the complications
associated with such a procedure. However, there is no evidence that early
tracheostomy reduces mortality or the rate of nosocomial pneumonia.
• The use of PI oral care is not recommended to reduce ventilator-
associated pneumonia and may cause an increased risk of acute respiratory
distress syndrome.
Level IIA
• Antimicrobial-impregnated catheters may be considered to prevent
catheter-related infections during external ventricular drainage.
Level III

45. BTF TBI 2017:Deep vein thrombosis
Prophylaxis
• LMWH or low-dose unfractioned heparin may be used in combination with
mechanical prophylaxis. However, there is an increased risk for expansion
of intracranial hemorrhage.
• In addition to compression stockings, pharmacologic prophylaxis may be
considered if the brain injury is stable and the benefit is considered to
outweigh the risk of increased intracranial hemorrhage.
• There is insufficient evidence to support recommendations regarding the
preferred agent, dose, or timing of pharmacologic prophylaxis for deep vein
thrombosis.
Level III

46. BTF TBI 2017: Seizure prophylaxis
• Prophylactic use of phenytoin or valproate is not recommended for
preventing late PTS.
• Phenytoin is recommended to decrease the incidence of early PTS (within
7 d of injury), when the overall benefit is thought to outweigh the
complications associated with such treatment. However, early PTS have
not been associated with worse outcomes.
• At the present time there is insufficient evidence to recommend
levetiracetam compared with phenytoin regarding efficacy in preventing
early post-traumatic seizures and toxicity.
Level IIA

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