Traumatic Brain Injury — Part 4: Specific Injury Types, Herniation & Advanced Monitoring
Epidural hematoma, acute and chronic subdural hematoma, traumatic subarachnoid hemorrhage, diffuse axonal injury, skull fractures, penetrating TBI, cerebral herniation syndromes, and advanced neuromonitoring including PbtO2, cerebral microdialysis, continuous EEG, and transcranial Doppler.
1. Epidural Hematoma (EDH)
1.1 Epidemiology and Pathophysiology
Epidural hematomas occur in approximately 1–4% of all TBI patients and up to 10% of patients with severe TBI. They result from hemorrhage between the dura mater and the inner table of the skull.1
| Feature | Detail |
|---|---|
| Most common source | Middle meningeal artery (80–90% of cases), typically from a temporal bone fracture |
| Venous sources | Dural venous sinuses (especially posterior fossa EDH), diploic veins, middle meningeal vein |
| Associated skull fracture | Present in 75–95% of adult EDH (less frequent in children, whose skulls are more pliable) |
| Most common location | Temporal region (60–70%), frontal (20%), posterior fossa (5–10%), vertex (rare) |
| Age distribution | Peak incidence age 20–30; uncommon in patients > 60 (dura is more adherent to skull) and infants < 2 years |
1.2 Clinical Presentation
| Pattern | Description | Frequency |
|---|---|---|
| Classic lucid interval | LOC at impact → transient improvement (“lucid interval”) → rapid deterioration | ~20–30% of cases |
| Never loses consciousness | Alert throughout; deterioration heralded by headache, vomiting, drowsiness | ~30% |
| Never regains consciousness | LOC at impact without recovery; often associated with other intracranial injuries | ~30% |
| Delayed presentation | Symptoms develop hours to days after injury (venous or slow arterial bleeding) | ~10% |
Danger Signs Indicating Expansion:
- Declining GCS (≥ 2 points)
- Ipsilateral pupil dilation (uncal herniation from temporal EDH)
- Contralateral hemiparesis
- Cushing response (hypertension, bradycardia)
1.3 Management
Surgical indications for EDH are detailed in Part 3, Section 4.1. Key points.
- Surgical EDH: Craniotomy with hematoma evacuation and middle meningeal artery cauterization. Bone flap is typically replaced.
- Nonoperative EDH: Close monitoring in a neurosurgical center with serial CT imaging (at 6–8 hours, 24 hours, and then as clinically indicated). Thresholds for surgical intervention should be low given the risk of rapid deterioration.
Time is Brain in EDH: Epidural hematoma is the most time-sensitive surgical lesion in TBI. Mortality rises dramatically with delay in surgical evacuation after onset of pupillary dilation. Patients with acute EDH and anisocoria should be in the operating room within 1–2 hours of presentation.1
2. Subdural Hematoma (SDH)
2.1 Acute Subdural Hematoma (aSDH)
Pathophysiology
Acute SDH results from tearing of bridging veins that span the subdural space between the cortical surface and the dural venous sinuses. Unlike EDH, aSDH is frequently associated with significant underlying brain injury (contusion, DAI), which accounts for its higher mortality.2
| Feature | Detail |
|---|---|
| Mechanism | Acceleration-deceleration injury tears bridging veins; direct cortical vessel disruption |
| Associated injuries | Cortical contusion (> 50%), DAI, cerebral edema |
| Risk factors for aSDH | Falls in elderly (especially on anticoagulants), high-energy mechanism in young adults, brain atrophy (increased bridging vein stretch) |
| CT appearance | Crescent-shaped, hyperdense (60–80 HU) collection conforming to brain surface; crosses suture lines but does not cross the midline (stops at falx) |
| Mortality | 40–60% overall; up to 90% in patients presenting with bilateral fixed dilated pupils |
Surgical Management
Surgical indications are detailed in Part 3, Section 4.2.
| Feature | Detail |
|---|---|
| Surgical approach | Large trauma craniotomy (≥ 12 cm); dural opening; evacuation of clot; meticulous hemostasis of cortical surface |
| Decompressive component | If significant brain swelling is present intraoperatively, consider leaving the bone flap off (converting to hemicraniectomy with duraplasty) |
| Subdural drain | Placed postoperatively to prevent recurrence |
| Timing | Every effort should be made to operate within 4 hours of injury. For patients with GCS ≤ 8 and pupillary abnormalities, surgery within 2 hours is the goal |
2.2 Chronic Subdural Hematoma (cSDH)
| Feature | Detail |
|---|---|
| Definition | SDH present for ≥ 3 weeks; often 4–8 weeks post-injury |
| Pathophysiology | Organized hematoma with neomembrane formation; repeated microhemorrhages from friable neomembrane vessels; gradual enlargement |
| Population | Predominantly elderly; those on anticoagulants; patients with brain atrophy, alcohol use disorder, CSF shunts |
| Mechanism | Often trivial or no recalled trauma (up to 50% of cases) |
| CT appearance | Hypodense (< 25 HU, older blood) or isodense or mixed-density (if recurrent bleeding into chronic collection); crescent shape |
| MRI appearance | T1 hyperintense, T2 variable; distinguishes from hygroma |
Management of Chronic SDH
| Treatment | Indication |
|---|---|
| Observation | Small, asymptomatic cSDH; incidental finding; closely follow with serial CT |
| Burr hole drainage | Most common surgical treatment; one or two burr holes with irrigation and subdural drain placement. Success rate ~80–90%3 |
| Craniotomy | For organized/septated collections that cannot be adequately drained through burr holes; recurrent cSDH after burr hole drainage |
| Middle meningeal artery embolization (MMAE) | Emerging treatment to reduce recurrence after surgical drainage; targets the neomembrane blood supply. The EMBOLISE trial and subsequent studies show reduced recurrence rate.4 |
| Dexamethasone | The Dex-CSDH trial (2020) showed that dexamethasone did NOT improve outcomes and was associated with more adverse events. NOT recommended as primary treatment5 |
Recurrence Rate: 10–20% after initial burr hole drainage. Risk factors for recurrence include bilateral cSDH, midline shift > 10 mm, septated collection, coagulopathy, and advanced age.
3. Traumatic Subarachnoid Hemorrhage (tSAH)
3.1 Characteristics
Traumatic SAH is the most common finding on CT in patients with moderate-to-severe TBI, present in approximately 30–40% of all TBI patients with CT abnormalities.6
| Feature | Detail |
|---|---|
| Pathophysiology | Disruption of small pial or cortical vessels; blood in the subarachnoid space (sulci, cisterns, fissures) |
| Distribution | Typically convexity sulci and Sylvian fissures (in contrast to aneurysmal SAH, which concentrates in basal cisterns) |
| Prognostic significance | Independent predictor of worse outcome in TBI; associated with higher ICP and worse GCS |
3.2 Management Differences from Aneurysmal SAH
| Feature | Traumatic SAH | Aneurysmal SAH |
|---|---|---|
| Cause | Mechanical disruption of pial/cortical vessels | Aneurysm rupture |
| Distribution on CT | Convexity, sulci, Sylvian fissures | Basal cisterns (perimesencephalic, suprasellar) |
| Cerebral vasospasm | Occurs in ~20–40% but less frequently symptomatic; peaks days 2–5 | Occurs in ~70%; peaks days 4–14; major cause of morbidity |
| Nimodipine | NOT routinely indicated; may cause hypotension that worsens cerebral perfusion | Standard of care (60 mg q4h × 21 days) |
| Angiography | NOT indicated unless distribution suggests aneurysmal pattern or mechanism inconsistent with trauma | Mandatory (CTA followed by DSA if needed) |
| ICP management | Per TBI protocol (see Part 3) | Per SAH protocol |
| Seizure prophylaxis | Per TBI protocol (7 days) | Variable; often 7 days |
Clinical Pearl: If the pattern of SAH on CT suggests a basal cistern distribution (suprasellar, ambient, prepontine) in a trauma patient, ALWAYS consider underlying aneurysm rupture as the cause of the fall/MVC. Obtain CTA to rule out an underlying vascular lesion.6
4. Diffuse Axonal Injury (DAI)
4.1 Pathophysiology
DAI results from rotational acceleration-deceleration forces that cause shearing of axons, particularly at interfaces between tissues of different density (gray-white matter junction, corpus callosum, brainstem). It is the most common cause of persistent unconsciousness and disability after TBI.7
| Grade | Location | CT Findings | MRI Findings (SWI/DWI) | Prognosis |
|---|---|---|---|---|
| Grade I (Mild) | Gray-white matter junction (lobar white matter) | Often normal | Punctate hemorrhagic or non-hemorrhagic lesions at gray-white junction | Better prognosis; persistent neuropsychological deficits common |
| Grade II (Moderate) | Corpus callosum (especially splenium and body) | May show hemorrhagic foci in corpus callosum | Lesions in corpus callosum ± lobar white matter | Intermediate prognosis |
| Grade III (Severe) | Brainstem (dorsolateral midbrain, pons) | May show brainstem hemorrhage (Duret hemorrhage) | Lesions in brainstem + corpus callosum + lobar white matter | Poor prognosis; prolonged coma; high mortality or severe disability |
4.2 Diagnosis
| Modality | Utility |
|---|---|
| CT | Low sensitivity (< 25%) for DAI; may appear normal or show only small petechial hemorrhages at gray-white junction |
| MRI with SWI (susceptibility-weighted imaging) | Most sensitive imaging modality for hemorrhagic DAI; demonstrates microhemorrhages as hypointense “blooming” foci |
| MRI with DWI (diffusion-weighted imaging) | Detects non-hemorrhagic (cytotoxic edema) DAI lesions within hours of injury |
| MRI with DTI (diffusion tensor imaging) | Quantifies white matter tract integrity (fractional anisotropy); used primarily in research and chronic TBI assessment |
4.3 Management
DAI management is primarily supportive; there is no specific surgical treatment.7
- Optimize cerebral perfusion (avoid hypotension, hypoxia)
- ICP management per protocol if elevated (though ICP may be normal in isolated DAI)
- Seizure prophylaxis
- Prolonged rehabilitation with expectation of slow recovery over months to years
- MRI lesion burden (number and location of lesions) is the strongest imaging predictor of long-term outcome
5. Skull Fractures
5.1 Linear Skull Fractures
| Feature | Detail |
|---|---|
| Definition | Non-displaced fracture line through the calvarium |
| Significance | By itself, generally benign; however, indicates significant force was applied. Fractures crossing the middle meningeal artery groove or dural venous sinuses increase risk of epidural hematoma |
| Management | Observation; admit if associated intracranial pathology. No specific treatment for the fracture itself |
| Growing skull fracture (pediatric) | A linear fracture in a child < 3 years may expand over time if dura is torn and leptomeninges herniate through the defect. Follow-up imaging is recommended for young children with skull fractures |
5.2 Depressed Skull Fractures
Surgical indications are detailed in Part 3, Section 4.3.
| Feature | Detail |
|---|---|
| Open vs. closed | Open: overlying scalp laceration with communication to the fracture site. Closed: scalp intact |
| Degree of depression | Measured relative to the inner table of adjacent intact skull. Depression > full thickness of the skull = surgical indication |
| Risk of infection | Open depressed fractures: 2–5% without antibiotics; < 1% with prophylactic antibiotics and surgical debridement |
| Seizure risk | Higher than other fracture types; prolonged seizure prophylaxis may be warranted |
5.3 Basilar Skull Fractures
| Feature | Detail |
|---|---|
| Definition | Fracture involving the base of the skull (anterior, middle, or posterior fossa) |
| Clinical signs | These are primarily clinical diagnoses, as basilar fractures are frequently not visible on standard axial CT |
Classic Clinical Signs:
| Sign | Description | Location Suggested |
|---|---|---|
| Raccoon eyes (periorbital ecchymosis) | Bilateral periorbital ecchymosis without direct orbital trauma | Anterior fossa fracture |
| Battle sign (mastoid ecchymosis) | Ecchymosis over the mastoid process; appears 12–72 hours after injury | Middle/posterior fossa fracture (petrous bone) |
| CSF rhinorrhea | Clear watery drainage from the nose; positive for β-2 transferrin (gold standard test) or glucose > 30 mg/dL (less specific) | Anterior fossa (cribriform plate, frontal sinus) |
| CSF otorrhea | Clear watery drainage from the ear | Middle fossa (tegmen tympani, petrous bone) |
| Hemotympanum | Blood behind the tympanic membrane (seen on otoscopy) | Petrous bone fracture |
| Cranial nerve palsies | CN VII (facial nerve) and CN VIII (hearing loss) most common; CN I (anosmia) with anterior fossa fractures | Varies by location |
| Pneumocephalus | Air in the intracranial space on CT | Communication between sinuses/mastoid air cells and intracranial space |
Management of Basilar Skull Fractures:
| Issue | Management |
|---|---|
| CSF leak | Most (70–80%) resolve spontaneously within 7–10 days. Elevate HOB 30°; avoid straining, nose blowing, and Valsalva. If persistent > 7–10 days, consider lumbar drain. Surgical repair for refractory leaks |
| Meningitis prophylaxis | Prophylactic antibiotics for basilar skull fracture with CSF leak are controversial. Most evidence does NOT support routine prophylactic antibiotics; they may select for resistant organisms. Consider antibiotics only for persistent CSF leak > 7 days or contaminated wounds8 |
| Nasal intubation | Absolutely contraindicated in suspected anterior fossa basilar skull fracture — risk of intracranial passage through the cribriform plate |
| Nasogastric tube | Contraindicated in anterior fossa fracture — use orogastric tube instead |
| CN VII palsy | If immediate onset: may indicate nerve transection (worse prognosis; consider surgical exploration). If delayed onset: usually neuropraxia from edema (good prognosis; steroids may be considered) |
| Hearing loss | Conductive (ossicular disruption): may benefit from surgery. Sensorineural (cochlear/CN VIII damage): typically permanent |
5.4 Skull Fracture Summary Table
| Type | CT Finding | Key Risk | Management |
|---|---|---|---|
| Linear | Non-displaced fracture line | EDH if crossing vascular groove | Observation |
| Depressed (closed) | Bone below inner table level | Underlying parenchymal injury | Surgery if depression > skull thickness, neuro deficit, or intracranial hematoma |
| Depressed (open) | Bone below inner table + scalp laceration | Infection, meningitis | Surgical debridement, elevation, antibiotics |
| Basilar | May be subtle; pneumocephalus, fluid in sinuses/mastoid | CSF leak, CN injury, meningitis | Conservative for most; surgical repair for persistent CSF leak |
| Growing (pediatric) | Widening linear fracture over time | Leptomeningeal herniation | Surgical repair |
6. Penetrating TBI
6.1 Epidemiology and Pathophysiology
Penetrating TBI accounts for approximately 10% of all TBI-related deaths and carries an overall mortality of 70–90% for gunshot wounds to the head.9
| Feature | Detail |
|---|---|
| Gunshot wounds | Most common cause of penetrating TBI; high-velocity projectiles create a permanent cavity (tissue destruction along projectile path) and temporary cavity (radial displacement of surrounding tissue) |
| Stab wounds | Lower velocity; damage largely confined to wound tract |
| Blast injuries | Fragments, shrapnel; multiple small penetrating injuries possible |
6.2 Management Principles
| Principle | Detail |
|---|---|
| Airway | Early intubation (GCS ≤ 8 or declining); avoid nasal intubation if anterior skull base involvement |
| Do NOT remove impaled objects | Stabilize in place until neurosurgical exploration in OR; removal may cause fatal hemorrhage |
| CT imaging | Non-contrast CT of head; CT angiography if trajectory near major vascular structures (carotid, vertebral arteries, sagittal sinus) |
| Surgical exploration | Debridement of accessible devitalized tissue, bone fragments, and accessible projectile. Deep-seated projectiles that are not easily accessible should generally NOT be pursued surgically (risk of additional damage exceeds benefit) |
| Dural repair | Watertight closure to prevent CSF leak and infection |
| Antibiotics | Broad-spectrum prophylaxis: cefazolin 2 g IV q8h + metronidazole 500 mg IV q8h (or per institutional protocol); duration 5–7 days |
| Seizure prophylaxis | Strongly recommended; penetrating TBI has the highest risk of post-traumatic epilepsy (30–50% lifetime risk)10 |
| Anticoagulation reversal | As indicated |
| ICP management | Per standard protocol; EVD preferred for monitoring + drainage |
| Vascular injury | CTA mandatory for projectile trajectories crossing vascular territories; angiography and endovascular treatment for traumatic pseudoaneurysm or arteriovenous fistula |
6.3 Prognostic Factors
| Factor | Outcome |
|---|---|
| GCS 3–5 with bilateral fixed dilated pupils | > 95% mortality; many centers consider nonoperative management |
| Bihemispheric or transventricular trajectory | > 80% mortality |
| GCS > 8 with unilateral or tangential wound | Better prognosis; aggressive treatment warranted |
| Posterior fossa wounds | High mortality from brainstem injury |
7. Advanced Neuromonitoring
7.1 Brain Tissue Oxygen Monitoring (PbtO2)
Rationale
ICP monitoring alone provides information about pressure but not about tissue oxygenation. Brain tissue oxygen (PbtO2) monitoring uses a small catheter (Licox or Raumedic) placed in the frontal white matter to directly measure the partial pressure of oxygen in brain tissue.11
| Parameter | Detail |
|---|---|
| Normal PbtO2 | 25–35 mmHg |
| Treatment threshold | PbtO2 < 20 mmHg — indicates cerebral hypoxia requiring intervention |
| Critical threshold | PbtO2 < 10 mmHg — severe cerebral ischemia; associated with poor outcomes |
| Target | PbtO2 ≥ 20 mmHg |
BOOST Trials
| Trial | Design | Key Finding |
|---|---|---|
| BOOST-2 (Phase 2, 2017) | ICP + PbtO2 monitoring vs. ICP alone in severe TBI | PbtO2-guided therapy reduced brain tissue hypoxia (fraction of monitoring time with PbtO2 < 20 mmHg) without increasing adverse events; trend toward improved outcomes12 |
| BOOST-3 (Phase 3, ongoing) | Definitive trial evaluating whether PbtO2-guided therapy improves long-term outcomes | Enrollment completed; results pending |
Interventions for Low PbtO2
| Intervention | Mechanism |
|---|---|
| Increase FiO2 | Increases arterial oxygen content |
| Optimize CPP (increase MAP or decrease ICP) | Improves cerebral perfusion |
| Increase hemoglobin (transfuse if Hgb < 7–9) | Improves oxygen-carrying capacity |
| Reduce cerebral metabolic demand (deeper sedation, temperature control) | Decreases oxygen consumption |
| Optimize PaCO2 (avoid excessive hyperventilation) | Prevents vasoconstriction-induced ischemia |
7.2 Jugular Venous Oxygen Saturation (SjvO2)
| Parameter | Detail |
|---|---|
| Method | Retrograde catheter placed in the internal jugular vein (dominant side) with tip at the jugular bulb |
| Normal SjvO2 | 55–75% |
| SjvO2 < 50% | Cerebral ischemia (increased extraction) — increase CPP, increase FiO2, reduce hyperventilation |
| SjvO2 > 75% | Hyperemia or cell death (decreased extraction/utilization) — may indicate infarction if persistent |
| Limitations | Global measure (may miss regional ischemia); catheter malposition common; continuous monitoring requires calibration |
7.3 Cerebral Microdialysis
| Parameter | Detail |
|---|---|
| Method | Small dialysis catheter placed in frontal white matter; samples interstitial fluid for metabolic markers |
| Key markers | Glucose, lactate, pyruvate, glutamate, glycerol |
| Lactate/pyruvate ratio (LPR) | > 25 — metabolic distress; > 40 — severe metabolic crisis |
| Low cerebral glucose | < 0.7 mmol/L — cerebral energy failure; may prompt glucose or insulin adjustment |
| Elevated glycerol | Cell membrane breakdown — indicates ongoing injury |
| Clinical utility | Primarily research tool; available at specialized centers. Helps detect cerebral energy crisis that may not be apparent from ICP or PbtO2 alone13 |
7.4 Continuous EEG (cEEG) Monitoring
| Indication | Detail |
|---|---|
| Unexplained decreased consciousness | Particularly when clinical exam is disproportionately poor relative to imaging |
| After clinical seizure | To confirm seizure resolution and detect nonconvulsive status epilepticus (NCSE) |
| During neuromuscular blockade | MANDATORY — seizures cannot be detected clinically in paralyzed patients |
| Barbiturate coma | To confirm burst suppression pattern and titrate dose |
| Refractory ICP | To detect subclinical seizures as a contributing cause |
Nonconvulsive Seizures in TBI:
| Finding | Detail |
|---|---|
| Prevalence in severe TBI | 20–30% of patients with severe TBI have subclinical (nonconvulsive) seizures on cEEG14 |
| Impact | Increases cerebral metabolic demand → worsens secondary injury; associated with worse outcomes |
| Detection | Requires continuous EEG; standard intermittent (routine) EEG has low sensitivity |
| Treatment | Standard antiepileptic therapy; may require continuous infusion (midazolam, propofol, or pentobarbital) for nonconvulsive status epilepticus |
7.5 Transcranial Doppler (TCD)
| Parameter | Detail |
|---|---|
| Method | Pulsed-wave Doppler through transtemporal acoustic window; measures flow velocity in middle cerebral artery (MCA) and other intracranial vessels |
| Mean flow velocity (MFV) | Normal: 55 ± 12 cm/sec in MCA |
| Pulsatility index (PI) | Normal: 0.6–1.1; PI > 1.4 suggests elevated ICP or distal vascular resistance |
| MFV > 120 cm/sec (MCA) | Vasospasm (in context of tSAH) or hyperemia |
| Lindegaard ratio | MCA MFV / extracranial ICA MFV. Ratio > 3 = vasospasm; Ratio > 6 = severe vasospasm |
| Low MFV with high PI | Suggests elevated ICP with decreased cerebral perfusion |
| Absent diastolic flow → reverberating flow → absent flow | Progressive signs of cerebral circulatory arrest (used as ancillary test for brain death) |
Uses of TCD in TBI:
| Application |
|---|
| Noninvasive estimation of ICP and CPP (screening, not replacement for invasive monitoring) |
| Detection of vasospasm in traumatic SAH |
| Assessment of cerebral autoregulation (transient hyperemic response test) |
| Ancillary test for brain death determination |
| Monitoring during acute deterioration when invasive monitoring not yet placed |
7.6 Optic Nerve Sheath Diameter (ONSD)
| Parameter | Detail |
|---|---|
| Method | Point-of-care ultrasound measurement of the optic nerve sheath diameter 3 mm behind the globe |
| Normal | < 5.0 mm |
| Elevated ICP suggested | ONSD > 5.0 mm (some studies use > 5.7 mm) |
| Sensitivity/specificity for elevated ICP | ~90%/85% (varies by study and threshold) |
| Utility | Screening tool for elevated ICP in settings without invasive monitoring; NOT a substitute for EVD/intraparenchymal monitor |
| Limitations | Operator-dependent; affected by orbital pathology; provides binary information (elevated or not) rather than continuous ICP values15 |
8. Neurosurgical Consultation Criteria
Neurosurgical consultation should be obtained promptly for any of the following.1 16
| Indication |
|---|
| GCS ≤ 12 with abnormal CT |
| Any intracranial hemorrhage requiring potential surgical evacuation |
| Epidural hematoma (any size, given potential for rapid expansion) |
| Acute subdural hematoma > 5 mm or any SDH with midline shift |
| Depressed skull fracture (open or with depression > skull thickness) |
| Penetrating head injury |
| Posterior fossa hematoma |
| ICP monitoring and EVD placement |
| Deteriorating neurological examination attributable to intracranial pathology |
| Intraparenchymal hemorrhage > 20 mL or with mass effect |
| Bilateral temporal contusions (high risk for rapid deterioration) |
| CSF leak persistent > 7 days |
| Growing skull fracture in pediatric patients |
9. Brain Death Determination in TBI
When TBI results in devastating neurological injury and brain death is suspected, a structured evaluation is required.17
9.1 Prerequisites
| Prerequisite | Requirement |
|---|---|
| Known cause | Irreversible cause of coma established (clinical and imaging consistent with devastating brain injury) |
| Core temperature | ≥ 36°C (≥ 96.8°F) |
| Systolic blood pressure | ≥ 100 mmHg |
| No confounding medications | Drug levels below therapeutic threshold for sedatives, analgesics, and paralytics. Pharmacologic neuromuscular blockade must be excluded (TOF ≥ 4/4) |
| No severe metabolic derangement | Normal electrolytes; pH > 7.28; glucose 70–300 mg/dL |
| Observation period | Typically ≥ 24 hours from insult; shorter if imaging demonstrates devastating injury (e.g., massive hemorrhage with herniation) |
9.2 Clinical Examination
| Test | Finding Consistent with Brain Death |
|---|---|
| Coma | No eye opening or motor response to noxious stimulation (central and peripheral) |
| Pupillary reflex | Both pupils fixed and dilated (≥ 4 mm); no response to bright light |
| Corneal reflex | Absent bilaterally |
| Oculocephalic reflex (doll’s eyes) | Absent (eyes remain fixed relative to orbits during head turning; only test if cervical spine cleared) |
| Oculovestibular reflex (cold calorics) | No eye deviation with 50 mL ice water instilled into each ear canal (after confirming intact tympanic membranes) |
| Gag reflex | Absent |
| Cough reflex | Absent with deep tracheal suctioning |
| Apnea test | No respiratory effort with PaCO2 ≥ 60 mmHg AND ≥ 20 mmHg above baseline (performed after preoxygenation; 100% O2 delivered via tracheal catheter during test) |
9.3 Ancillary Tests (When Clinical Exam Cannot Be Completed)
| Test | Finding |
|---|---|
| Cerebral angiography | Absence of intracranial blood flow |
| Radionuclide perfusion scan (Tc-99m HMPAO) | No cerebral uptake (“empty skull” or “hollow skull” sign) |
| Transcranial Doppler | Reverberating flow, systolic spikes, or absent flow |
| EEG | Electrocerebral silence (not required in most US protocols but used in some countries) |
Regulatory Note: Brain death determination requirements vary by state and country. Always follow local institutional policy and applicable legal standards. Most US states require one or two examinations separated by a defined interval (typically 6–24 hours), performed by qualified physicians.17
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Aarabi B, Tofighi B, Kufera JA, et al. “Predictors of outcome in civilian gunshot wounds to the head.” J Neurosurg. 2014;120(5):1138-1146. DOI: 10.3171/2014.1.JNS131869 ↩︎
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Okonkwo DO, Shutter LA, Moore C, et al. “Brain tissue oxygen monitoring and management in severe traumatic brain injury (BOOST-2).” Crit Care Med. 2017;45(11):1907-1914. DOI: 10.1097/CCM.0000000000002619 ↩︎
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ACS TQIP. “ACS TQIP Best Practices in the Management of Traumatic Brain Injury.” American College of Surgeons. 2015. URL: https://www.facs.org/quality-programs/trauma/quality/best-practices-guidelines/ ↩︎
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