traumatic brain injury

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)

4. 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

5. 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

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

7.  GENERAL PATHOPHYSIOLOGY:
initial phases
second stage
 SPECIFIC PATHOPHYSIOLOGY:
CEREBRAL BLOOD FLOW
HYPOPERFUSION AND HYPERPERFUSION
CEREBROVASCULAR AUTOREGULATION AND CARBON DIOXIDE
(CO2) REACTIVITY
CEREBRAL VASOCONSTRICTION.
CEREBRAL METABOLIC DYSREGULATION:
OXIDATIVE STRESS AND EXCITOTOXICITY:

8. CEREBRAL TISSUE EDEMA:
INFLAMMATION
NECROSIS VS APOTOSIS:

9. DIAGNOSTICS IN TBI
GCS:1976

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

11. 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

12. 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

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

14. 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

15. 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

16. 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

17. 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.

18. 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

19. 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.

20. 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.

21.  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.

22. 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.

23. 8. 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.
 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

24.  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..

25.  10. Deep Vein Thrombosis Prophylaxis
 Low molecular weight heparin (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

26. 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

27. 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)



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

29. 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.

30. 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.

31. 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.