This document provides an overview of traumatic brain injury (TBI), including causes, types, diagnosis, management guidelines, and the Lund therapy protocol. Some key points: 1. Road traffic accidents and falls are the leading causes of TBI. Common types include skull fractures, contusions, hemorrhages, and diffuse axonal injury. 2. Diagnosis involves assessing Glasgow Coma Scale and using imaging like CT, MRI to identify fractures and lesions. Biomarkers in fluid can also help. 3. Management guidelines address issues like decompressive craniectomy, ventilation, hyperosmolar therapy, barbiturates, nutrition, and maintaining cerebral perfusion pressure. 4. The

1. TRAUMATIC BRAIN INJURY
What really matters!!!
Riyadh Abdullah Almogahed
ICU resident AQSH.

2. THE INCREDIBLE STORY OF HOLT

3. Traumatic brain injury (TBI)
1-a non-degenerative, non-congenital insult to
brain from an External mechanical force,
2-permanent or temporary impairment of
physical, and psychosocial functions, diminished
altered state of consciousness.
3-(GCS)(1) within 48 hours as being severe GCS=
8, moderate GCS = 9-12, mild GCS= 13-15. (2)

5. Modes of injuries to the brain include:
Road Traffic Accidents "RTA“ 50%.
Falls 20-30% of total cases of TBIs. Persons aged 75 years and
older . Pediatric age group also frequently withstands TBI due to
falls.
Firearms cause 12% of TBI
Occupation related TBIs cause 45-50% of all TBIs.
Drug abuse and Alcohol are main causes of TBIs and are often
associated with the leading causes of TBI namely RTAs, and fall
from heights

6. PATHOLOGY OF TBI:
(1) Primary injury, which takes place
immediately after trauma
(2) Secondary injury, a process which starts
at the time after trauma and produces
effects that may continue for a long time

7. TYPES OF TBI:
SKULL FRACTURES
CONTUSIONS “COUP AND COUNTERCOUP”
INTRACRANIAL HEMORRHAGES:
EDH/SDH/ICH/SAH/IVH
CONCUSSION
DIFFUSE AXONAL INJURY

9. DIAGNOSTICS IN TBI
GCS:1976

11. DIAGNOSTICS IN TBI
SKULL RADIOGRAPH
CT BRAIN : BONE WINDOW,BRAIN WINDOW, SUBDURAL
WINDOW
MRI, MRA, MRV
ANGIOGRAPHY
FLUID BIOMARKERS !

12. Midline shift Cisterns High or mixed density lesion Notes
I None Present None No visible pathology on CT scan
II 0-5 mm Present None
III 0-5mm
Compressed or
absent
None Swelling
IV >5 mm None
V Any Any Any Any lesion surgically evacuated
VI >25 cm cubic Not surgically evacuated
Marshall CT classification in Traumatic brain injury

13. ADRENERGIC HYPERACTIVITY:
TBI in particular leads to immediate and profound SNS activation with
massive release of both central and peripheral catecholamine.
Detrimental effect on cardiovascular, respiratory, inflammation.
 Paroxysmal Sympathetic Hyperactivity:
1-Hyperthermia;
2-Tachycardia;
3-Tachypnea;
4-Agitation,
5-Diaphoresis.
6-Dystonia

14. GUIDELINES FOR THE MANAGEMENT OF
SEVERE TRAUMATIC BRAIN INJURY
4TH EDITION SEPTEMBER 2016

16. MANAGEMENT OF TRAUMATIC BRAIN INJURY
1.Decompressive Craniectomy:

A LARGE frontotemporoparietal DC is
recommended over a small frontotemporoparietal
DC for reduced mortality and improved neurologic
outcomes in patients with severe TBI

17. 2.Prophylactic Hypothermia
Early (within 2.5 hours), short-term (48 hours post-injury)
prophylactic hypothermia is not recommended to improve
outcomes in patients with diffuse injury

18.  3. Hyperosmolar Therapy
While mannitol was previously
thought to reduce intracranial
pressure through simple brain
dehydration, both mannitol and
hypertonic saline work to reduce
intracranial pressure, at least in
part, through reducing blood
viscosity, leading to improved
microcirculatory flow of blood
constituents and consequent
constriction of the pial arterioles,
resulting in decreased cerebral
blood volume and intracranial
pressure

19. 3. Hyperosmolar Therapy
Although hyperosmolar therapy may lower intracranial
pressure, there was insufficient evidence about effects
on clinical outcomes to support a specific
recommendation, or to support use of any specific
hyperosmolar agent, for patients with severe traumatic
brain injury.

20. 4. Cerebrospinal Fluid Drainage
 An EVD” external ventricular drainage” 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 Glasgow Coma Scale (GCS) <6
during the first 12 hours after injury may be considered

21. 5. Ventilation Therapies
 Normal ventilation is
currently the goal for severe
TBI patients in the absence of
cerebral herniation and normal
partial pressure of carbon
dioxide in arterial blood
(PaCO2) ranges from 35-45
mm Hg.

22. 5. Ventilation Therapies
 Low PaCO2, therefore, results in low CBF and may result
in cerebral ischemia while high PaCO2 levels can result in
cerebral hyperemia and high intracranial pressure (ICP).
Therefore, providing optimal CBF is important under
normal and abnormal conditions.
Prolonged prophylactic hyperventilation with partial
pressure of carbon dioxide in arterial blood (PaCO2) of 25
mm Hg or less is not recommended.

23.  6. Anesthetics, Analgesics, and Sedatives
 • 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.

25. 7. 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.

26. 8. Nutrition
 Feeding patients to attain basal caloric replacement at
least by the 5th day and, at most, by the seventh day
post-injury is recommended to decrease mortality.
 Transgastric jejunal feeding is recommended to reduce
the incidence of ventilator-associated pneumonia.
 A moderate approach to insulin therapy should be
adopted as the practice of “tight glucose control” could
have deleterious effects in patients with severe TBI

27.  9. Infection Prophylaxis
Early tracheostomy is recommended to reduce
mechanical ventilation days. However, there is no evidence
that early tracheostomy reduces mortality or the rate of
nosocomial pneumonia.
The use of povidone-iodine oral care is not recommended
to reduce VAP and may cause an increased risk of acute
respiratory distress syndrome.
 Antimicrobial-impregnated catheters may be considered to
prevent catheter-related infections during EVD..

28.  10. Deep Vein Thrombosis Prophylaxis
 Low molecular weight heparin
(LMWH) or unfractioned heparin may be
used in combination with mechanical
prophylaxis.
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.


29.  11. 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 days of injury).
At the present time there is
insufficient evidence to recommend
levetiracetam over phenytoin
regarding efficacy in preventing
early post-traumatic seizures and
toxicity

30. 15. Blood Pressure Thresholds
 Maintaining systolic blood
pressure SBP at ≥100 mm Hg
for patients 50 to 69 years old or
at ≥110 mm Hg or above for
patients 15 to 49 or over 70 years
old may be considered to
decrease mortality and improve
outcomes. (211)



31. 16. Intracranial Pressure
Thresholds
Treating ICP above 22 mm Hg
is recommended because values
above this level are associated
with increased mortality. (211)

32. 17. Cerebral Perfusion Pressure Thresholds:
 The recommended target cerebral perfusion pressure
(CPP) value for survival and favorable outcomes is
between 60 and 70 mm Hg.
Avoiding aggressive attempts to maintain CPP above 70
mm Hg with fluids and vasopressors may be considered
because of the risk of adult respiratory failure.

33. THE LUND THERAPY:
 1) Stress reduction with adequate sedation and
catecholamine blockade;
 2) Maintenance of euvolemia through the use
of erythrocyte transfusion and maintenance of
a normal albumin level;
 3) Preservation of cerebral perfusion pressure
(60–70 mm Hg for adults and 40–55 mm Hg
for children and adolescents);
 4) Avoidance of cerebrospinal drainage;
 5) Use of early nutrition; and
 6) Use of mechanical ventilation to promote
normal oxygenation and ventilation.

36. THE LUND THERAPY:
In part the protocol advocated by the group from Lund emphasizes the
use of metoprolol, a selective beta1- antagonist, and clonidine, an
alpha 2-agonist, which are used to limit the posttraumatic
hyperadrenergic stress response.
Combined, these drugs can be used to lower MABP, hypothetically
reducing capillary hydrostatic pressure to the point where fluid filtration
halts and reabsorption can occur.
Although this induced reduction in MABP may lower cerebral perfusion
pressure, the Lund group has used hemodynamic (247) and microdialysis
data to suggest that this effect is well tolerated by patients with brain
injuries.