This is a simple description on how to manage a traumatic brain injury patient in short.

1. Peri-operative
Management of
Traumatic Brain
Injury
Dr. S. M. Farhad Sazib
RMO Neuro ICU

2. Cornerstones of TBI management
Recognition of mass lesions
Prompt detection
evacuation
ICP management
Head positioning
Sedation/neuromuscular blockade
CSF drainage
Osmotherapy
Barbiturates
Decompressive craniectomy
Hyperventilation
Cerebral perfusion
CPP management
Adequate oxygenation
Avoidance of hypotension/hypoxia
Neuroprotective strategies

3. Recognition of mass lesions

4. Types of structural primary brain injury
Focal
• Hematoma
- Epidural
- Subdural
- Intracerebral
• Contusion
• Concussion
• Lacerations
Diffuse
• Concussion
• Multifocal contusion
•Diffuse axonal injury

5. Concussion
• Alteration of
consciousness
without structural
damage as a result of
non penetrating
traumatic brain injury
(TBI).

6. Contusion
TBI with CT findings that may include:
• low attenuation areas: representing associated edema
• high attenuation areas (AKA "hemorrhagic contusions"): usually
produce less mass effect than their apparent size. Most common in
areas where sudden deceleration of the head causes the brain to
impact on bony prominences (e.g. temporal, frontal and occipital
poles). These areas may progress to frank parenchymal hemorrhages.
Surgical decompression may sometimes be considered if herniation
threatens

7. Contusion

8. Diffuse Axonal Injury
• A primary lesion of rotational acceleration/deceleration head injury
• May be diagnosed clinically when loss of consciousness (coma) lasts >
6 hours in absence of evidence of intracranial mass or ischemia
• In its severe form, hemorrhagic foci occur in the corpus callosum and
dorsolateral rostral brain stem with microscopic evidence of diffuse
injury to axons (axonal retraction balls, microglial stars, and
degeneration of white matter fiber tracts).

9. Diffuse Axonal Injury

10. Epidural hematoma
• EDH volume > 30 cm3 should be evacuated regardless of GCS
• EDH with the all of the following characteristics can be managed
nonsurgically: 1) with serial CT scans and close neurological
observation in a neurosurgical center: volume < 30 cm3 and thickness
< 15 mm and with midline shift (MLS) < 5 mm and GCS>9 and no focal
neurologic deficit
• patients with an acute EDH and GCS ≤ 9 and anisocoria undergo
surgical evacuation ASAP

11. Epidural hematoma

12. Subdural hematoma: Acute
• ASDH with thickness > 10 mm or midline shift (MLS) > 5 mm (on CT)
should be evacuated regardless of GCS
• ASDH with thickness < 10 mm and MLS < 5 mm should undergo
surgical evacuation if: GCS drops by 2 points from injury to admission
and/or the pupils are asymmetric or fixed and dilated and/or ICP is>
20 mm Hg
• monitor ICP in all patients with ASDH and GCS < 9

13. Subdural hematoma: Acute

14. Subdural hematoma: Chronic
• Surgical evacuation of hematoma indicated for: symptomatic lesions:
including focal deficit, mental status changes or subdurals with
maximum thickness greater than 1 cm
• Complications of surgery: seizures, intracerebral hemorrhage (ICH),
failure of the brain tore-expand and/or reaccumulation of the
subdural fluid, tension pneumocephalus, subdural empyema

15. Subdural hematoma: Chronic

16. Other forms of TBI
• Skull fractures
• Pneumocephalus
• Traumatic subdural hygroma
• Extra axial fluid collections in children
• Post traumatic hydrocephalus
• Gunshot wounds to the head
• Non missile penetrating brain trauma
• High altitude brain edema

17. Cerebral perfusion

18. Outcomes from TBI
Primary Injury
Secondary
Injury process
Secondary Ischemic insults
Intracranial
hypertension
Cerebral
ischemia
Delivery
Consumption
•Fever
•seizures
Global Regional
CBF
•ICP ↑
•BP↓
•pCO2↓
•vasospasm
Arterial
oxygen
Concentration
•Anemia
•hypoxia

19. Relation between CPP, ICP and MAP

20. Control of CPP to avoid ischemia
CMRO2 = CBF x AVDO2
• CMRO2 = Cerebral metabolic rate of oxygen in mL/100g/min
• CBF = cerebral blood flow in mL/100g/min
• AVDO2 =Arteriovenous difference in oxygen (measured by jugular
venous oxygen content SjvO2 from systemic arterial oxygen content)

21. CPP autoregulation

22. Distortion of the autoregulation

23. Initial assessment
This should involve
• evaluation of airway, breathing and circulation
• a rapid assessment of neurological status and
• associated extracranial injuries as well as
• evaluation of anemia
• coagulopathy
• glycemia and
• the presence of adequate vascular access

24. Initial assessment (continued)
• Information about time and mechanism of injury can be valuable
• Brief neurological assessment is performed using Glasgow Coma Scale
(GCS) score and pupillary responses
• Associated thoracic, abdominal, spinal and long bone injuries may be
stable or evolve during the perioperative period and must be
considered in differential diagnosis of new onset hypotension,
anemia, hemodynamic instability or hypoxemia during anesthesia and
surgery

25. Airway management
Airway management in TBI is complicated by a number of factors
including
• urgency of situation (because of pre-existing or worsening hypoxia)
• uncertainty of cervical spine status
• uncertainty of airway (due to presence of blood, vomitus, debris in
the oral cavity or due to laryngo-pharyngeal injury or skull base
fracture)
• full stomach
• intracranial hypertension and
• uncertain volume status

26. Airway management (continued)
• The anterior portion of the cervical collar may be removed when
manual in-line stabilization is established
• Nasal intubation should be avoided in patients with base of skull
fracture
• It is advisable to have a back-up plan ready in case of difficult
intubation
• Sodium thiopental, etomidate and propofol decrease cerebral
metabolic rate for O2 and attenuate increases in ICP with intubation
• The choice of muscle relaxant for rapid sequence induction is
between succinylcholine and rocuronium

27. Ventilation
• Ventilation should be adjusted to ensure adequate oxygenation (PaO2
> 60 mmHg) and normocarbia (PaCO2 35-45 mmHg)
• Hyperventilation should be used judiciously for short-term control of
ICP and to facilitate surgical exposure during craniotomy
• Excessive and prolonged hyperventilation may cause cerebral
vasoconstriction leading to ischemia
• Normocarbia should be restored before dural closure
• It is ideal to monitor cerebral oxygenation and CBF during prolonged
hyperventilation
• Hyperventilation should be avoided during the first 24 h after injury
when CBF is often critically reduced.

28. Blood pressure management
• Brain Trauma Foundation guidelines for the management of TBI
recommend avoiding hypotension (SBP < 90 mmHg) and maintaining
CPP between 50 and 70 mmHg
• Hypotension during craniotomy also contributes to adverse outcomes
and is frequently encountered at the time of dural opening
• This “decompression hypotension” may be predicted by low GCS
score, absence of mesencephalic cisterns on CT and B/L dilated pupils
• The presence of multiple CT lesions, subdural hematoma, maximum
thickness of CT lesion and longer duration of anesthesia increase the
risk for intraoperative hypotension

29. Vasopressors and their role in cerebral
hemodynamics

30. Intravenous fluids
• Mannitol therapy is often immediately initiated in patients suspected
of intracranial hypertension with impending signs of herniation
• Hypertonic saline may be beneficial resuscitation fluid for TBI patients
because it increases intravascular fluid and decreases ICP
• Warm, non-glucose containing isotonic crystalloid solution is
preferable for intravenous administration in TBI patients

31. Blood transfusion
• Anemia is associated with increased in-hospital mortality and poor
outcome in TBI
• Anemia may cause cerebral injury via various possible mechanisms
including tissue hypoxia, reactive oxygen species induced damage,
inflammation, disruption of blood-brain barrier (BBB) function,
vascular thrombosis and anemic cerebral hyperemia
• It may also impair cerebral autoregulation

32. Blood transfusion (continued)
• A number of cerebroprotective physiological mechanisms become
effective with anemia which include aortic chemoreceptor activation,
increased sympathetic activity leading to increased heart rate, stroke
volume and cardiac index, reduced systemic vascular resistance, and
enhanced oxygen extraction
• A number of cellular mechanisms of cerebral protection become
effective. These include increased Hypoxia Inducible Factor (HIF),
nitric oxide synthase and nitric oxide in the brain erythropoietin and
vascular endothelial growth factor (VEGF) mediated angiogenesis and
vascular repair

33. Blood transfusion (continued)
• Besides increasing the oxygen-carrier capacity of blood, red blood cell
transfusion increases the circulating volume and can increase CBF in
patients with impaired cerebral autoregulation secondary to the TBI
• However, most studies have failed to demonstrate a consistent
improvement in brain tissue oxygenation (PbtO2) with blood
transfusion
• In fact, the increased hematocrit after red cell transfusion may
potentially decrease CBF and increase the risk of cerebral ischemia
• There is no benefit of a liberal transfusion strategy (transfusion when
Hb <10 g/dl) in moderate to severe TBI

34. ICP management

35. Rosner’s vasodilatory cascade
CPP ↓
Vasodilation↑
CBV ↑
ICP ↑

36. Reduction of ICP: stepwise approach
Elevate head of bed to 30 degrees;
head in neutral position, avoid
cervical venous compression
Maintain normocapnia (PCO2 goal 35-
40 mmHg)
Adequate sedation
CSF drainage by
ventriculostomy
Osmotherapy
Neuromuscular
paralysis
If refractory consider -
High dose barbiturate therapy
Hyperventilation
Decompressive hemicraniectomy

37. Regarding sedation in TBI
• Ketamine was traditionally avoided in the management of patients
with TBI due to concerns that it increased ICP
• A systematic review demonstrated that ICP did not increase in any of
the studies during ketamine administration
• The antagonism of NMDA receptors by ketamine can decrease the
release of neurotoxic glutamate and may impart a protective effect in
patients with traumatic brain injury
• Dexmedetomidine has favorable effects on heart rate, blood
pressure, and agitation making a useful sedation agent in vented TBI
patients

38. Cerebrovascular profiles of commonly used
sedatives

39. Surgical options
• A large frontotemporoparietal decompressive craniectomy (not less
than 12 × 15 or 15 cm diameter) is recommended over a small
frontotemporoparietal craniectomy for reduced mortality and
improved neurologic outcomes in patients with severe TBI
• Bifrontal decompressive craniectomy is not recommended to improve
outcomes
• An EVD system zeroed at the midbrain with continuous drainage of
CSF may be considered to lower ICP burden more effectively than
intermittent use
• Another option can be cisternostomy

40. Regarding anesthetic techniques
• Intravenous anesthetic agents including thiopental, propofol and
etomidate cause cerebral vasoconstriction and reduce CBF, cerebral
blood volume, cerebral metabolic rate for O2(CMRO2) and ICP
• Opioids have no direct effects on cerebral hemodynamics when the
ventilation is controlled
• All volatile anesthetic agents decrease CMRO2 but may cause cerebral
vasodilation, resulting in raised ICP
• At less than 1 minimum alveolar concentration (MAC) concentration,
the cerebral vasodilatory effects are minimal
• Nitrous oxide should be avoided since it increases CMRO2 and causes
cerebral vasodilation and increased ICP

41. Other issues

42. Coagulopathy
• Coagulation disorders may be present in approximately one-third TBI
patients and is associated with an increased mortality and poor
outcome
• Patients with GCS ≤8, Injury Severity Score (ISS) ≥ 16, associated
cerebral edema, subarachnoid hemorrhage and midline shift are likely
to have coagulopathy
• Use of tranexamic acid has been found to be associated with a
reduction of mortality

43. Nutrition
• TBI results in a hypermetabolic state that increases systemic and
cerebral energy requirements
• Early enteral nutrition within first week of TBI with adjustment of
glycemia showed improved outcome and reduced mortality
• Feeding patients to attain basal caloric replacement at least by the
fifth day and, at most, by the seventh day post injury is recommended
by updated guidelines
• Transgastric jejunal feeding is recommended to reduce the incidence
of ventilator-associated pneumonia.

44. Glycemic control
• Hyperglycemia after TBI is associated with increased morbidity and
mortality
• Hyperglycemia can cause secondary brain injury, leading to increased
glycolytic rates evidenced by increased lactate/pyruvate ratio,
resulting in metabolic acidosis within brain parenchyma,
overproduction of reactive oxygen species, and ultimately neuronal
cell death
• Tight glucose control with intensive insulin therapy remains
controversial.

45. Glycemic control (continued)
• Intraoperative hyperglycemia is common in adults undergoing
urgent/emergent craniotomy for TBI with up to 15% patients
experiencing New Onset Hyperglycemia
• It may be predicted by severe TBI, the presence of subdural
hematoma, preoperative hyperglycemia, and age ≥ 65 years
• Perioperative hyperglycemia during craniotomy for TBI is common in
children
• TBI severity and the presence of subdural hematoma predict
intraoperative hyperglycemia in pediatric cases

46. Infection prophylaxis
• Infection risk is considered to be high in TBI patients
• Respiratory tract infections are the most common among TBI
patients, with a notable predominance of Acinetobacter reported as a
ventilator-associated pneumonia (VAP) pathogen
• Tracheostomy is recommended to reduce mechanical ventilation days
to avoid ventilator deconditioning in patients
• The use of povidone-iodine in oral care is not recommended to
reduce VAP
• PI oral care has been associated with an increased risk of acute
respiratory distress syndrome

47. Seizure prophylaxis
• In patients with severe TBI, the rate of clinical post-traumatic seizures
(PTS) may be as high as 12%, while that of subclinical seizures
detected on electroencephalography may be as high as 20 to 25%
• PTS are classified into early when < 7 days or late when they occur
after 7 days
• Seizures often occur as result of hematoma formation, presence of
retained foreign body, depressed skull fractures, GCS score less than
10, and amnesia
• Phenytoin is recommended to decrease the incidence of early PTS
• Prophylactic use of phenytoin or valproate is not recommended for
preventing late PTS. Levetiracetam can be better in that case.

48. DVT prophylaxis
• Low-dose unfractionated heparin or LMWH may be used in
combination with mechanical prophylaxis once the intracranial
hemorrhage is stable
• There is a potential risk for expansion of intracranial hemorrhage so
the appropriate time to initiate anticoagulation would be based on
clinical guidance
• Options for mechanical prophylaxis are compression stockings,
sequential compression device

49. Paradoxical sympathetic storm
• Characterized by episodic hyperhidrosis, hypertension, hyperthermia,
tachypnea, tachycardia and posturing
• Only suggested after exclusion of mass lesions, seizure,
toxic/metabolic derangements and infections
• Represent disruption of autonomic function in the diencephalon and
brain stem
• A combination of small doses of morphine for sedation and
appropriate α1 and β receptor blockade with labetalol is particularly
effective

50. Therapeutic hypothermia
• Hypothermia was believed to reduce cerebral metabolism during
stress, reduces excitatory neurotransmitters release, attenuates BBB
permeability
• But in recent studies, The use of hypothermia is associated with an
increased incidence of adverse events (e.g., coagulopathy,
immunosuppression, and cardiac dysrhythmia) and a lack of
improvement in outcome compared to normothermic patients.

51. References
• Handbook of neurosurgery – Greenberg
• Perioperative Management of Adult Traumatic Brain Injury, Deepak
Sharma, MD and Monica S. Vavilala, MD, Anesthesiol Clin. 2012 June ;
30(2): 333–346. doi:10.1016/j.anclin.2012.04.003
• Perioperative Management of Severe Traumatic Brain Injury: What Is
New? Deacon Farrell & Audrée A. Bendo
https://doi.org/10.1007/s40140-018-0286-1
• Operative neurosurgical techniques – Schmidek and Sweet
• Youngman’s Neurological Surgery
• Neurocritical care - Lori Shutter, Bradley Molyneaux, John A. Kellum

52. Thank you