Traumatic Brain Injury (TBI)

 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.

 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

 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(increased metabolism)
• Hyperglycemia / hypoglycemia
• Pyrexia

# Key principle in ICU: Prevent secondary brain injury

 Classification of TBI

A. By Severity (Glasgow Coma Scale)

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

 Initial Assessment — ATLS Approach

1.Primary Survey (ABCDE)

2. Neuroimaging in TBI

Non-contrast CT Head

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

MRI Brain

• DAI
• Brainstem injury
• Prognostication (later)

 Raised Intracranial Pressure (ICP)

Normal ICP

• Adults: 7–15 mmHg in horizontal position
• An ICP value >20 mmHg is considered abnormal, while levels exceeding 25 mmHg warrant urgent and aggressive intervention, as they are associated with a high risk of secondary brain injury.
• The gold standard technique for ICP monitoring is the use of an external ventricular drain (EVD)-diagnostic and therapeutic . This device is inserted into the ventricular system, typically at the level of the foramen of Monro.

Raised ICP Pathophysiology

• Brain edema
• Hematoma
• Impaired CSF drainage
• Acute hypoxemia (for example, due to a respiratory infection) leads to cerebral vasodilation, which increases cerebral blood flow (CBF).
• Impaired venous drainage can also occur due to intracranial causes, such as injury to the venous sinuses
• External compression of the neck (e.g., tight cervical collars) can obstruct jugular venous outflow
• Positive pressure ventilation raises intrathoracic pressure, reducing cerebral venous return
• Elevated intra-abdominal pressure (seen in conditions like constipation or even during patient transport when heavy objects rest on the abdomen) can indirectly increase venous pressure and ICP

Monroe–Kellie Doctrine

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

 Cerebral Perfusion Pressure (CPP)

CPP = MAP − ICP

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

In patients with traumatic brain injury (TBI), positioning and pressure referencing are crucial for accurate hemodynamic assessment.

Most TBI patients are nursed with the head elevated to 30°, Because of the vertical height difference between the heart and the head in a 30° head-up position, there can be a pressure gradient of ~10–11 mmHg. As a result, referencing MAP at the right atrium will overestimate cerebral perfusion pressure (CPP).

Therefore, both:

• ICP transducer, and
• Arterial pressure transducer (MAP)

must be zeroed at the level of the external auditory meatus (tragus)—which approximates the level of the brain.

 ICU Management of Severe TBI 

A. Airway & Ventilation

• Indications for intubation
• GCS ≤ 8
• Airway compromise
• Target:(From Taable of Text Book Of Critical care)

 Blood Pressure (SBP targets – age specific)

👉 Prevent even a single episode of hypotension

B. Hemodynamic Management

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

C. ICP Control — Tier Wise(Different in different guidelines)

 First-tier

• Head elevation 30°
• Neutral neck-Loosen collar – improve venous drainage
• Analgesia + sedation
• Normoxia, normocapnia
• Normoglycemia
• Treat fever
• CSF drainage (EVD)

Traditionally, the use of lumbar CSF drainage in patients with raised intracranial pressure was avoided due to concern for brain herniation (“coning”). The rationale was that removing cerebrospinal fluid from the spinal compartment could create a pressure gradient between the cranial and spinal compartments, potentially precipitating downward displacement of brain structures.

However, more recent experience suggests that this risk may have been overestimated, particularly in carefully selected patients. As a result, lumbar drains are increasingly being utilized in some centers as an adjunct for managing refractory intracranial hypertension, especially when conventional therapies have failed.

 Second-tier

• Osmotherapy
• Mannitol (0.25–2 g/kg)-mannitol can precipitate out in the cold,higher incidence of renalcomplications
• Hypertonic saline(3% 3–5 mL/kg)
• Hyperventilation

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(e.g. a blown pupil) to buy a few extra minutes 
• As a bridge to definitive therapy (surgery / osmotherapy)

—> Never maintain PaCO₂ < 30 mmHg

Third-tier

• Barbiturate coma
• Decompressive craniectomy
• Targeted hypothermia (NO BENEFIT -Eurotherm study)

Decompressive Craniectomy in TBI (Refractory Intracranial Hypertension)

1. DECRA trial

• Population: Diffuse TBI
• Intervention trigger: ICP >20 mmHg for >15 minutes despite initial therapy
• Comparison: Standard care (including barbiturates) vs early DC

Findings:

• DC effectively reduced ICP
• However, it resulted in worse functional neurological outcomes

 Critical interpretation:

• The ICP threshold (20 mmHg) and short duration (15 min) were likely too low, leading to premature surgery

2. RESCUEicp trial

• Population: Severe TBI with refractory ICP
• Intervention trigger: ICP >25 mmHg for 1–12 hours
• Comparison: Medical therapy vs DC

Findings:

• Mortality reduction: ~22 additional survivors per 100 patients in the surgical group
• BUT → Many survivors had severe disability / poor quality of life

 Key dilemma:

• Survival vs neurological outcome
• Raises ethical concerns regarding acceptable outcomes and patient selection

Coagolopathy

Traumatic brain injury (TBI) can also trigger trauma-induced coagulopathy (TIC). As a result, patients may develop a spectrum ranging from hypercoagulability (early) to hypocoagulability and bleeding tendency (later)

Use Point-of-care viscoelastic tests  which helps Early detection of coagulopathy → prevents hematoma expansion. 

Tranexamic acid (TXA)—-CRASH-3 trial,

1. Mortality Benefit (Time-Dependent)

• Reduced head injury–related death, especially in:
• Mild to moderate TBI (GCS 9–15)
• No significant benefit in:
• Very severe TBI (GCS 3–8)

 Earlier administration = better outcomes

2. Timing is Critical

• Benefit seen only if TXA given within 3 hours
• No benefit (may be harmful) if given late (>3 hours)

Dose 

• Loading dose: 1 g IV over 10 minutes
• Maintenance: 1 g IV infusion over 8 hours

Antiplatelet

patients who are already on antiplatelet therapy (e.g., aspirin, clopidogrel), routine platelet transfusion is not recommended For procedures such as craniotomy or decompressive surgery A target platelet count >100 × 10⁹/L .

Patients on Direct Oral Anticoagulants (DOACs) in TBI

• Dabigatran
  → Reversed by Idarucizumab
• Rivaroxaban (also apixaban, edoxaban)
  → Reversed by Andexanet alfa

Because of limited access to specific reversal agents, many centers rely on:

• Prothrombin Complex Concentrate (PCC)
  Fresh Frozen Plasma (FFP)
  → Less effective than PCC but still used where PCC is unavailable

Deep Vein Thrombosis Prophylaxis

Initial Strategy: Mechanical Prophylaxis First

• Start mechanical prophylaxis early in all patients unless contraindicated:
• Intermittent pneumatic compression (IPC) devices
• Compression stockings

 These reduce venous stasis without increasing bleeding risk

Pharmacological Prophylaxis (Anticoagulation)

• Major concern: hematoma expansion in brain
• Therefore, anticoagulation is delayed and individualized

Current Practical Approach (Guideline-Oriented Insight)

• Can be considered if repeat neuroimaging shows stable hemorrhage
• By 48–72 hours:initiate low molecular weight heparin (LMWH)

Role of IVC Filter

• Consider in:
• Very high VTE risk
• Contraindication to anticoagulation
• Prolonged immobilization

 Inferior vena cava filter prevents pulmonary embolism by trapping emboli from lower limbs

Albumin vs Saline

• Use of albumin for resuscitation in TBI has been shown to be harmful
• It is associated with increased mortality compared to normal saline

This finding is largely derived from the SAFE trial (TBI subgroup analysis)

Mechanism 

• Albumin is relatively hypotonic
• Can increase cerebral edema
• Leads to worsening ICP and poorer outcomes

Normal Saline vs Balanced Crystalloids

• Normal saline (0.9% NaCl) remains the standard fluid in TBI
• Despite theoretical benefits of balanced crystalloids (e.g., less hyperchloremia):

 No strong evidence shows superiority of balanced solutions over saline in TBI

sedatives (midazolam/propofol)

• First-line: Propofol infusion (if MAP stable)
• Avoid hypotension at all costs → may switch to midazolam
• Combine with analgesia (opioids like fentanyl)
• Aim for targeted sedation (not over-sedation)
• Consider escalation (e.g., barbiturates) in refractory ICP

Early vs Late Tracheostomy

Early Tracheostomy (≈ ≤7 days)

Potential Benefits:

• May reduce duration of mechanical ventilation
• Associated with shorter ICU length of stay
• Improved patient comfort and reduced sedation needs

Potential Downsides:

• Risk of performing the procedure in patients who may have recovered quickly
• Some evidence suggests delay in transfer to rehabilitation, possibly due to ongoing ICU-level care decisions

Decision = case-by-case, multidisciplinary

 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

# Complications of TBI

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

Prognostication in Traumatic Brain Injury (TBI)

— CLINICAL PROGNOSTIC FACTORS (MOST IMPORTANT)

 A. Glasgow Coma Scale (GCS)

• Strongest early predictor

 Limitations:

• Sedation, paralysis, intoxication confound

 B. Pupillary Reactivity 

 Bilateral non-reactive pupils → suggests:

• Brainstem dysfunction
• Raised ICP / herniation

 C. Age

Mechanism:

• Reduced neuroplasticity
• More comorbidities

 D. Hypotension & Hypoxia (SECONDARY INSULTS)

• SBP <90 mmHg → doubles mortality
• Hypoxia (PaO₂ <60 mmHg) → major predictor of poor outcome

 Preventing secondary injury = strongest modifiable prognostic factor

 E. Motor Response (GCS Motor Score)

• Best component of GCS
• Extensor/no response → poor outcome

 — CT-BASED PROGNOSTICATION

 Marshall CT Classification

 Rotterdam CT Score (More Accurate)

Components:

• Basal cisterns
• Midline shift
• Epidural lesion
• IVH/SAH

 Higher score = worse prognosis

4. INTRACRANIAL PRESSURE (ICP) & PHYSIOLOGY

• Sustained ICP >22 mmHg → poor outcome
• CPP <60 mmHg → cerebral ischemia → poor outcome

 Pressure Reactivity Index (PRx)

• Reflects autoregulation

Brain Tissue Oxygen (PbtO₂) <20 mmHg → worse outcomes

 5. MRI FINDINGS

Key Predictors:

• Diffuse Axonal Injury (DAI):
• Grade III (brainstem) → very poor prognosis
• Brainstem lesions → worst outcomes
• Corpus callosum involvement → severe injury

6. BIOMARKERS 

 Not standalone tools yet (guidelines: adjunct only)

 7. ELECTROPHYSIOLOGY

 EEG

• Non-reactive EEG → poor prognosis
• Status epilepticus → worse outcomes

 Somatosensory Evoked Potentials (SSEP)

• Bilateral absent N20 → poor prognosis

8. PROGNOSTIC MODELS 

 IMPACT Model

(International Mission for Prognosis and Analysis of Clinical Trials)

Variables:

• Age
• GCS motor
• Pupils
• CT findings
• Hypoxia, hypotension

 CRASH Model

(Corticosteroid Randomisation After Significant Head Injury)

Predicts:

• 14-day mortality
• 6-month outcome

 Widely used in research & clinical estimation

 9. OUTCOME SCALES

 Glasgow Outcome Scale (GOS)

 Extended GOS (GOSE)

• More granular (8 categories)

 10. TIMING OF PROGNOSTICATION

 Always:

• Correct confounders (sedation, hypothermia)
• Avoid early withdrawal decisions

REFFERENCE-OHS MANUAL, text book of critical care