Traumatic Brain Injury (TBI)

1️⃣ Definition

Traumatic Brain Injury (TBI) is an alteration in brain function or evidence of brain pathology caused by an external mechanical force, leading to temporary or permanent neurological impairment.

Alteration in brain function includes: loss of consciousness, amnesia, confusion, focal neurological deficit, or change in mental state.

2️⃣ Epidemiology & Importance

  • Major cause of death and disability worldwide
  • Common in young adults (road traffic accidents) and elderly (falls)
  • Significant ICU burden → prolonged ventilation, raised ICP, secondary brain injury


3️⃣ Pathophysiology of TBI

A. Primary Brain Injury (At the moment of impact)

Occurs immediately and is non-reversible

Mechanisms

  • Direct impact (coup–contrecoup)
  • Acceleration–deceleration
  • Rotational forces

Types

  • Cerebral contusion
  • Laceration
  • Diffuse axonal injury (DAI)
  • Skull fractures
  • Intracranial hematomas


B. Secondary Brain Injury (Minutes → days)

Potentially preventable & treatable

Mechanisms

  • Hypoxia
  • Hypotension
  • Hypercapnia / hypocapnia
  • Raised ICP → ↓ CPP
  • Excitotoxicity (↑ glutamate)
  • Mitochondrial dysfunction
  • Neuroinflammation
  • Cerebral edema
  • Seizures
  • Hyperglycemia / hypoglycemia
  • Pyrexia

# Key principle in ICU: Prevent secondary brain injury


4️⃣ Classification of TBI

A. By Severity (Glasgow Coma Scale)

Severity

GCS Score

Mild

13–15

Moderate

9–12

Severe

≤8


B. By Morphology (Imaging Based)

🔹 Extra-axial Lesions

  • Epidural hematoma (EDH)
  • Subdural hematoma (SDH)
  • Subarachnoid hemorrhage (tSAH)

🔹 Intra-axial Lesions

  • Cerebral contusion
  • Intracerebral hemorrhage
  • Diffuse axonal injury


5️⃣ Common Intracranial Lesions 

—>Epidural Hematoma (EDH)

  • Arterial bleed (middle meningeal artery)
  • Lucid interval
  • Biconvex (lens-shaped) on CT
  • Rapid deterioration → neurosurgical emergency


—> Subdural Hematoma (SDH)

  • Venous bleed (bridging veins)
  • Crescent-shaped
  • Elderly, alcoholics, anticoagulated
  • Acute / subacute / chronic


—> Diffuse Axonal Injury (DAI)

  • Rotational injury
  • Normal CT possible
  • MRI (SWI/DTI) diagnostic
  • Common cause of persistent coma


6️⃣ Glasgow Coma Scale (GCS)

Component

Score

Eye Opening

1–4

Verbal Response

1–5

Motor Response

1–6

Total

3–15

# Motor score is most prognostic


7️⃣ Initial Assessment — ATLS Approach

🔹 Primary Survey (ABCDE)

  • A: Airway with cervical spine protection
  • B: Breathing, oxygenation
  • C: Circulation, control hypotension
  • D: Disability (GCS, pupils)
  • E: Exposure (look for other injuries)


8️⃣ Neuroimaging in TBI

Non-contrast CT Head

  • First-line investigation
  • Rapid, available
  • Detects fractures, bleeds, mass effect

MRI Brain

  • DAI
  • Brainstem injury
  • Prognostication (later)


9️⃣ Raised Intracranial Pressure (ICP)

Normal ICP

  • Adults: 5–15 mmHg

Raised ICP Pathophysiology

  • Brain edema
  • Hematoma
  • Impaired CSF drainage

Monroe–Kellie Doctrine

Total intracranial volume =Brain +  Blood +  CSF (constant)


🔟 Cerebral Perfusion Pressure (CPP)

CPP = MAP − ICP

Parameter

Target

ICP

< 22 mmHg

CPP

60–70 mmHg

#Hypotension (SBP < 100–110 mmHg) is strongest predictor of mortality


1️⃣ ICU Management of Severe TBI 

A. Airway & Ventilation

  • Indications for intubation
    • GCS ≤ 8
    • Airway compromise
  • Target:
    • PaO₂ > 60 mmHg
    • SpO₂ > 94%
    • PaCO₂ 35–40 mmHg

Avoid ->Prolonged hyperventilation → cerebral ischemia


B. Hemodynamic Management

  • Avoid hypotension
  • Maintain MAP to achieve CPP ≥ 60
  • Balanced crystalloids preferred


C. ICP Control — Stepwise

🔹 First-tier

  • Head elevation 30°
  • Neutral neck
  • Analgesia + sedation
  • Normoxia, normocapnia
  • Normoglycemia
  • Treat fever

🔹 Second-tier

  • Osmotherapy
    • Mannitol (0.25–1 g/kg)
    • Hypertonic saline
  • CSF drainage (EVD)

Hyperventilation belongs to the SECOND-TIER therapy for raised intracranial pressure (ICP) in severe traumatic brain injury.


🔹 Why SECOND-TIER?

  • Hyperventilation causes ↓ PaCO₂
  • Leads to cerebral vasoconstriction
  • Results in ↓ cerebral blood volume → ↓ ICP

# Effect is rapid but temporary
# Causes reduced cerebral blood flow → risk of ischemia

Hence, it is NOT first-line.


 Current Guideline Position 

  • Avoid prophylactic hyperventilation
  • Target PaCO₂: 35–40 mmHg (normal ventilation)
  • Short-term hyperventilation (PaCO₂ 30–35 mmHg):
    • Only for acute neurological deterioration
    • As a bridge to definitive therapy (surgery / osmotherapy)

—> Never maintain PaCO₂ < 30 mmHg


🔹 Third-tier

  • Barbiturate coma
  • Decompressive craniectomy
  • Targeted hypothermia (select cases)


#Hyperosmolar Therapy 

Feature

Mannitol

Hypertonic Saline

Diuresis

Yes

Minimal

Hypotension risk

Yes

Less

Volume expansion

No

Yes

Serum Na monitoring

No

Yes


# Seizure Prophylaxis

  • Early post-traumatic seizures (≤7 days)
  • Levetiracetam or Phenytoin
  • Prophylaxis for 7 days only


# Temperature & Glycemic Control

  • Avoid fever (↑ CMRO₂)
  • Target glucose: 140–180 mg/dL
  • Tight control → hypoglycemia risk


# Nutrition

  • Early enteral feeding (within 24–48 h)
  • High-protein, hypercaloric
  • Prevent catabolism


# Prognostic Factors

Poor Prognostic Indicators

  • GCS ≤ 5
  • Bilateral fixed dilated pupils
  • Hypotension + hypoxia
  • DAI
  • Raised ICP refractory to therapy
  • Advanced age


# Complications of TBI

  • Raised ICP
  • Herniation syndromes
  • Neurogenic pulmonary edema
  • SIADH / Cerebral salt wasting
  • ARDS
  • Sepsis
  • Long-term cognitive & behavioral deficits