A rapid review for post graduate general surgery residents, for university exams

1. TRAUMATIC BRAIN
INJURY
Nabin Paudyal
Resident, General Surgery
Nobel Institute of Neurosciences

2. Introduction
• Major source of health loss and disability.
• Global burden of disease (GBD) study reports 2016
 Annual incidence  27.08 million
 Global prevalence: 55. million
 Increasing in countries with middle socio-demographic indices (21.8 %).
 Fall is the main mechanism of trauma followed by road traffic accidents.

3. What is TBI?
• Alteration in brain function or evidence of brain pathology, caused by an external
force.
• External force that may result in TBI include
 Head being struck by an object
 Head striking an object
 Acceleration-deceleration of the brain without direct external impact
 Penetration injury
 Blast/explosion
 Other forces yet to be defined.

4. Classification of TBI
• Can be classified in terms of clinical severity, mechanism of injury and
pathophysiology
• Classification on the basis of clinical severity scores:
A. Based on Glasgow Coma Scale (GCS)
 Mild injury (GCS of 13-15)
 Moderate injury (GCS 9-12)
 Less injury (GCS <8)
B. Full Outline of Unresponsiveness Score (FOUR score)

5. Classification of TBI
• Can be classified in terms of clinical severity, mechanism of injury and
pathophysiology
• Classification on the basis of clinical severity scores:
C. Neuroimaging scales:
1. Marshall Scale

6. Classification of TBI
• Can be classified in terms of clinical severity, mechanism of injury and
pathophysiology
• Classification on the basis of clinical severity scores:
C. Neuroimaging scales:
2. Rotterdam Scale

7. Pathophysiology of TBI-related brain
injury
• Current clinical approaches in the management of TBI revolves around
surgical treatment of primary brain injury lesions (subdural and epidural
hematomas) and identification, prevention and treatment of secondary brain
injury.
• Primary brain injury:
 At time of trauma
 Due to direct impact
 Acceleration/deceleration injury
 Penetration injury
 Blast waves
 Transfer of external mechanical forces to intracranial contents combination of focal
contusions, hematomas as well as shearing of white matter tracts (DAI)

9. Epidural hemorrhage
• Rupture of MMA a/w skull fracture
Subdural hemorrhage
Extra-axial hematomas
Rupture of bridging veins/ progression of
superficial cortical contusions

10. Sub-arachnoid hemorrhage
Following disruption of small pial vessels and occurs in sylvian fissures, interpeduncular
cisterns. Intraventricular hemorrhage and superficial ICH may also extend into subarachnoid
space
Extra-axial hematomas

11. Intraventricular hemorrhage
Following tearing of sub-ependymal veins or by extension from adjacent
intraparenchymal/ SAH.
Extra-axial hematomas

12. Pathophysiology of TBI-related brain
injury
• Secondary brain injury:
 Occurs due to molecular injury in the neurons initiated at the time of initial trauma and continue for hours or
days.
 Mechanisms during the secondary brain injury may be
 Neurotransmitter-mediated excitotoxicity causing glutamate, free radical injury to cell membranes
 Electrolyte imbalances
 Mitochondrial dysfunction
 Inflammatory responses
 Apoptosis
 Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury

13. Management of TBI
Focused to minimize effects of Primary Brain Injury

14. Initial evaluation and treatment
• Pre-hospital
 Prevent hypotension and hypoxia [associated with poor prognosis: OR 2.67 and 2.14
respectively]
 Pre-hospital airway management:
 Includes endotracheal intubation
 GCS <9
 SpO2 < 90 despite O2
 BP monitoring
 Prevention of hypotension
 Adequate fluid resuscitation using isotonic crystalloids
 Neurologic assessment
 Stabilize and immobilize spine during transport
 Consider spinal fracture and take precautions

15. Initial evaluation and treatment
• 1. Emergency department As per ATLS protocols
 ET intubation in patients with GCS <9, inability to protect airway, inability to maintain Spo2>90 despite
supplemental O2, patient with signs of herniation
 Vitals sings monitoring. Hypoxia, hypoventilation, hyperventilation and hypotension are avoided
 Assess for other systemic trauma as per ATLS protocol
 Detailed neurologic examination should be completed as soon as possible to determine the severity of TBI.
 ICP monitoring should begin in ED as soon as possible
 CBC, blood count, electrolytes, glucose, coagulation parameters, blood alcohol level and urine toxicology should
be checked.

16. • 2. Anti-fibrinolytic therapy
 Initiate tranexamic acid therapy within three hours of injury.
 Indicated for GCS >8 and <13.
 Tranexamic acid 1 gram infusion over 10 minutes, followed by IV infusion of 1
gram over eight hours

17. • 3. Neuroimaging
 A non-contrast CT Detect skull fractures,
intracranial hematomas, cerebral edema
 Obtain head CT in all patients with GCS 14 or
lower
 Follow up CT performed in instances of clinical
deterioration.
 In absence of clinical deterioration, repeat imaging
in 6 hours time in patients with hematoma
• 4. Screening for blunt cerebrovascular injury
 Rule out Blunt Cerebrovascular injury (BCVI)
[based on Denver Criteria]
 High risk patients for BCVI undergo multislice CT
angiography of head and neck
 Initiate Aspirin 81 mg in BCVI patients

18. Surgical Treatment
• Indications
 Low GCS scale
 Findings on head CT  hematoma volume
  thickness
  evidence of mass effect including midline shift

19. a. Extradural hematoma (EDH)
• Indications of surgery in EDH patients include
 Focal signs or symptoms attributable to EDH
 Coma [GCS<9] and pupillary abnormalities due to EDH
 Large hematoma volume (>30 ml)
 Hematoma causing elevated ICP or neurological deterioration.
• For patients who are awake and have no focal neurological deficits
 Hematoma >30 ml
 Clot thickness >15 mm
 Midline shift > 5mm
• Surgery technique Craniotomy with hematoma evacuation
 Craniectomy may be done in cases with significant cerebral edema or midline shift
• Timing Within 1 -2 hours after head trauma or the onset of neurologic deterioration
for comatose patients with acute EDH and signs of brain herniation

20. a. Extradural hematoma (EDH)
• Non-operative management
 Mild EDH patients (monitored in an inpatient setting)
 Thorough neurologic assessment (including GCS) should be performed every hourly
 Repeat CT scan within 7-8 hours after original CT scan
• Raised Intracranial pressure may require urgent intervention managed with
hematoma evacuation, hyperventilation and osmotic diuresis (mannitol or hypertonic
saline)

21. b. Subdural hematoma (SDH)
• Indications of surgery:
 >10mm in thickness
 Associated midline shift > 5mm on CT regardless of GCS
 GCS < or equal to 8
 GCS has decreased by> or equal to 2 points from the time of injury to hospital admission
 If patient has asymmetric or fixed and dilated pupils
 ICP > 20 mmHg
c. Intracerebral hemorrhage
• Indications of surgery:
 If posterior cranial fossa  Mass effect seen (obliteration of fourth ventricle, effacement of
basal cisterns, brain stem compression)
 If cerebral hemisphere hemorrhage >50 ml, GCS 6 to 8 with frontal or temporal hematoma
>20 ml with midline shift of 5mm and/or cisternal compression on CT scan

22. d. Depressed skull fracture
• Indications of surgery:
 Depression greater than the thickness of cranium
 Dural penetration
 Significant intracranial hematoma
 Frontal sinus involvement
 Cosmetic deformity
 Wound infection or contamination
 Pneumocephalus
e. Refractory intracranial hypertension
• Decompressive hemicraniectomy

23. Management in ICU
Prevention of Secondary brain injury

24. • Principal focus for severe TBI is to limit secondary brain injury.
• Treatment efforts are aimed at intracranial pressure management and maintenance of
cerebral perfusion
• BP management, temperature, blood glucose, seizure prevention are other important damage
preventive measures.

25. a. Hemodynamic monitoring
• Isotonic fluids to be used Normal saline preferred
 SMART-ICU trial no benefit seen in patients with balanced crystalloids
• Avoidance of hypotension should be the priority. Preferred SBP > 100 mmHg
• Cerebral perfusion pressure 60-70 mmHg is recommended
b. Ventilation
• Most patients are sedated and artificially ventilated
• ETCO2 monitoring should be used for monitoring in all ventilated patients
• PaO2 should be maintained above 60 mmHg.
• Hyperventilation should be avoided
• As increased PEEP is associated with increased ICP Maintain PEEP up to 15-20 cm H2O
in cases with ARDS with TBI

26. c. Antiseizure medications and EEG monitoring
• Antiseizure medications are generally recommended to prevent post traumatic
seizures.
• Levetiracetam is generally recommended.
• Duration Not established
• Used to prevent status epilepticus, systemic injury due to seizure, reduce/prevent raise
in ICP.
d. Venous thromboembolism prophylaxis
• Mechanical prophylaxis Intermittent pneumatic compression on admission
• Chemoprophylaxis UFH (5000 U) three times daily OR enoxaparin 40 mg OD

27. e. Management of glucose
• Avoid hypo- and hyperglycemia
• Target range of 140-180 mg/dl.
• Optimal recommended level of glucose has not been studied.
f. Temperature management
• Fever aggravates secondary brain injury, worsens ICP control
• Maintain normothermia
• Antipyretics, surface cooling devices
g. Nutritional management
• Nutritional supplementation should begin within five to seven days.
• Transpyloric enteral nutrition may be considered
• Early nutrition rates have shown to decrease rates of pneumonia, mortality and
hospital stay in some trials

28. Management of
Intracranial Pressure

29. Initial management
• Identify patients at risk of impending herniation
 Signs include pupillary asymmetry, unilateral or bilateral fixed and dilated pupil,
decorticate and decerebrate posturing, respiratory depression, Cushing triad (bradycardia,
irregular respiration, hypertension)

31. Prognosis
• Cohort studies show that patients
with severe head injury have 30
percent mortality risk
• 30-65 percentage of patients with
severe TBI will regain independence
• 5-15 percent patients with severe TBI
are discharged from acute care in
vegetative state
• Independent Risk factors for
prognosis:

32. Prognosis risk models
• CRASH prediction model • IMPACT model

33. Thankyou….