CEREBRAL CONTUSION 

Definition

A cerebral contusion is a focal traumatic parenchymal brain injury characterized by bruising of brain tissue with capillary bleeding, edema, and necrosis, most commonly involving the cortical gray matter and gray–white junction.

It represents a form of traumatic intracerebral hemorrhage (TICH) and often evolves dynamically over hours to days.

 

Epidemiology

  • Seen in 20–30% of moderate to severe TBI
  • Common in:
    • Road traffic accidents
    • Falls
    • Assaults
  • Frequently associated with:
    • Diffuse axonal injury (DAI)
    • Subdural hematoma
    • Skull fractures

 

Pathophysiology

1. Mechanism of Injury

A. Coup and Contrecoup Injury

  • Brain impacts the inner table of skull
  • Bony ridges (especially frontal and temporal fossae) cause parenchymal bruising

Site

Reason

Inferior frontal lobes

Rough orbital plates

Temporal lobes

Sphenoid ridge

Parietal lobes

Less common

Occipital lobes

Rare

 

2. Primary Injury

Occurs at the moment of trauma:

  • Capillary rupture
  • Petechial hemorrhages
  • Neuronal and glial damage
  • Disruption of BBB

 

3. Secondary Injury 

Progresses over hours–days:

  • Cerebral edema (vasogenic + cytotoxic)
  • Hemorrhagic progression of contusion (HPC)
  • Raised intracranial pressure (ICP)
  • Reduced cerebral perfusion pressure (CPP)
  • Ischemia and excitotoxicity
  • Inflammatory cascade

—> Key concept:Cerebral contusion is a dynamic lesion, not static.

 

Types of Cerebral Contusions

1. Based on Location

  • Frontal contusions (most common)
  • Temporal contusions (high risk of herniation)
  • Parietal contusions
  • Occipital contusions

 

2. Based on Pathology

  • Non-hemorrhagic contusion
  • Hemorrhagic contusion
  • Evolving contusion (most dangerous)

 

Clinical Features

1. General Features

  • Loss of consciousness
  • Headache
  • Vomiting
  • Confusion
  • Seizures (early post-traumatic)

 

2. Focal Neurological Deficits

Depend on location:

Location

Deficit

Frontal

Personality change, executive dysfunction

Temporal

Aphasia, memory loss, seizures

Parietal

Sensory deficits, neglect

Occipital

Visual field defects

 

3. Signs of Raised ICP

  • Worsening GCS
  • Bradycardia, hypertension (Cushing response)
  • Papilledema (late)
  • Pupillary asymmetry

 

Radiological Evaluation

CT Brain (First-line)

Acute CT Findings

  • Ill-defined hypodense area (edema)
  • Punctate or patchy hyperdensities (hemorrhage)
  • Commonly multiple
  • Surrounding edema

—> Temporal contusions are often underestimated early

 

Hemorrhagic Progression of Contusion (HPC)

  • Seen in 30–50%
  • Occurs within 24–72 hours
  • Risk factors:
    • Age >65
    • Coagulopathy
    • Antiplatelet/anticoagulant use
    • Hypotension
    • Large initial contusion

 

MRI Brain

  • More sensitive for:
    • Non-hemorrhagic contusions
    • DAI
  • SWI shows microbleeds
  • Not first-line in unstable patients

 

Severity Assessment

  • Glasgow Coma Scale (GCS)
  • Marshall CT classification
  • Rotterdam CT score
  • ICP trends and neurological deterioration

 

Management of Cerebral Contusion (NEURO-ICU FOCUSED)

Initial Management (ABCDE + Neuro-Protection)

Airway

  • Intubate if:
    • GCS ≤8
    • Airway compromise
    • Hypoxia

Breathing

  • Target:
    • PaO₂ >80 mmHg
    • Avoid hyperventilation (except impending herniation)

Circulation

  • Avoid hypotension (SBP ≥100–110 mmHg)
  • CPP target: 60–70 mmHg

 

Neuroprotective Strategies

1. ICP Control

General Measures

  • Head elevation 30°
  • Neutral neck position
  • Adequate sedation and analgesia

Osmotherapy

  • Mannitol 0.25–1 g/kg
  • Hypertonic saline (preferred in hypotension)

—> Avoid prophylactic osmotherapy

 

2. Seizure Prophylaxis

  • Indicated for:
    • Cortical contusions
    • Temporal lobe injury
  • Levetiracetam or Phenytoin
  • Duration: 7 days

 

3. Blood Pressure & CPP Management

  • Avoid hypotension at all costs
  • Vasopressors if needed (noradrenaline preferred)

 

4. Temperature Control

  • Maintain normothermia
  • Fever worsens secondary injury

 

5. Glycemic Control

  • Avoid hyperglycemia
  • Target 140–180 mg/dL

 

6. DVT Prophylaxis

  • Mechanical initially
  • Pharmacological once bleeding stabilized (usually after 24–48 h with stable CT)

 

Surgical Management

Indications for Surgery

  • Progressive neurological deterioration
  • Increasing contusion size with mass effect
  • Midline shift >5 mm
  • Refractory raised ICP
  • Large temporal contusions (high herniation risk)

Surgical Options

  • Decompressive craniectomy
  • Contusion evacuation
  • Lobectomy (rare, life-saving)

 

Complications

Early

  • Raised ICP
  • Herniation
  • Seizures
  • Expansion of hemorrhage

Late

  • Post-traumatic epilepsy
  • Cognitive impairment
  • Personality changes
  • Chronic subdural hematoma
  • Post-traumatic hydrocephalus

 

Prognosis

Depends on:

  • Age
  • GCS at presentation
  • Contusion volume and location
  • Secondary insults (hypoxia, hypotension)
  • ICP control

—> Temporal contusions carry worse prognosis

 

High-Yield Exam Pearls

  • Cerebral contusion is a dynamic lesion
  • Hemorrhagic progression occurs in up to 50%
  • Most common sites: frontal and temporal lobes
  • Early CT may underestimate severity
  • Seizure prophylaxis for 7 days
  • Avoid hypotension and hypoxia — strongest predictors of outcome
  • Large temporal contusions → early surgery

 

Key References (Exam-Standard)

  • Harrison’s Principles of Internal Medicine
  • Brain Trauma Foundation Guidelines
  • Irwin & Rippe’s Intensive Care Medicine
  • Vincent – Textbook of Critical Care
  • Adams & Victor’s Neurology
  • Neurocritical Care Society statements