Severe Traumatic Brain Injury & Contusions

ABPN Neurocritical Care Study Guide Exam

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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU

Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU

2 Chapter 2: Cerebral Physiology & Intracranial Dynamics

Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes

3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management

Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions

4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management

Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy

5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management

Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury

6 Chapter 6: Neuropharmacology, Analgesia & Sedation

ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU

7 Bleeding, Thrombosis & Hematologic Emergencies

Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity

8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine

Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention

9 Systemic Trauma & Environmental Injury

Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging

10 Cardiac Emergencies & Mechanical Support

IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies

11 Kidney Injury, Acid–Base & Renal Replacement

Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement

12 Systemic Infection & Endocrine Emergencies

Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies

13 Gastrointestinal & Hepatic Emergencies

Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects

14 Chapter 9: Neuroimaging in the Neuro-ICU

Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness

15 Chapter 10: Electrophysiology & Neuromonitoring

Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler

16 Angiography, Electrodiagnosis & CSF Analysis

Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage

17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria

Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria

18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies

Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction

19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage

Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH

20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia

Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations

21 Venous, Spinal & Traumatic Vascular Disease

Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury

22 Chapter 15: Traumatic Brain & Spinal Cord Injury

Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes

23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies

Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure

24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis

Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies

25 Neuroinflammation & Neurooncology

Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies

26 Pregnancy, Transplantation & Pediatric Care

Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care

27 Chapter 18: Neurosurgical & Perioperative Emergencies

Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies

28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU

Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor

Severe Traumatic Brain Injury & Contusions

Key Takeaways Explain This Topic AI

Primary brain injury results from immediate contact impact and rotational acceleration forces causing irreversible tissue laceration and axotomy, whereas secondary injury cascades (glutamate excitotoxicity, mitochondrial failure, free radical injury, and cerebral edema) represent the therapeutic targets of neurocritical care.

Brain Trauma Foundation (BTF) 4th Edition Guidelines mandate treating intracranial pressure (ICP) exceeding 22 mmHg, targeting a cerebral perfusion pressure (CPP) of 60 to 70 mmHg, and maintaining systolic blood pressure (SBP) at or above 100 mmHg (ages 50–69) or 110 mmHg (ages 15–49 or ≥ 70).

Surgical evacuation thresholds differ fundamentally: an epidural hematoma (EDH) requires emergent evacuation if volume exceeds 30 mL regardless of GCS, whereas an acute subdural hematoma (ASDH) mandates evacuation if thickness exceeds 10 mm or midline shift exceeds 5 mm regardless of GCS.

Diffuse axonal injury (DAI) results from angular shearing strains classified by Adams histopathology into Grade I (lobar white matter), Grade II (corpus callosum, particularly splenium), and Grade III (dorsolateral rostral brainstem), best visualized on MRI susceptibility-weighted imaging (SWI).

Post-traumatic seizure (PTS) prophylaxis with levetiracetam or phenytoin is indicated for exactly 7 days to suppress early post-traumatic seizures; it does not reduce late post-traumatic epilepsy and must be discontinued after day 7 if no clinical or electrographic seizures occur.

Last updated: October 2026

Severe Traumatic Brain Injury & Contusions

Severe traumatic brain injury ( T B I TBI TB I ), defined by a post-resuscitation Glasgow Coma Scale ( G C S GCS GCS ) score ≤ 8 \le 8 ≤ 8 , is a major cause of death and disability. Neurocritical care focuses on halting secondary injury while identifying surgical mass lesions requiring emergent operative decompression.

Biomechanical Forces and Primary vs. Secondary Injury Cascades

TBI evolves through two distinct pathophysiological phases:

Primary Brain Injury

Primary injury occurs at the instant of impact. Biomechanical mechanisms include contact impact (skull fractures, extradural hematomas, coup contusions) and rotational acceleration-deceleration forces (tissue shearing, subdural hematomas, diffuse axonal injury). These forces cause immediate, irreversible physical damage: parenchymal laceration, vascular disruption, and mechanical axotomy. Primary damage cannot be reversed; management focuses on secondary prevention and rapid surgical triage.

Secondary Brain Injury Cascades

Secondary injury evolves over hours to days, driven by systemic insults (hypotension, hypoxemia, hyperthermia, hypercapnia) and cellular cascades:

Glutamate Excitotoxicity: Massive depolarization and impaired astrocytic uptake cause extracellular glutamate accumulation. Overactivation of N M D A NMDA NM D A and A M P A AMPA A MP A receptors drives massive intracellular calcium ( C a 2 + Ca^{2+} C a 2 + ) and sodium ( N a + Na^+ N a + ) influx.

Mitochondrial Dysfunction: Intracellular C a 2 + Ca^{2+} C a 2 + overload collapses the mitochondrial membrane potential, opens the permeability transition pore ( m P T P mPTP m PTP ), arrests A T P ATP A TP synthesis, and releases cytochrome c to trigger apoptosis.

Free Radical Injury: Impaired electron transport generates reactive oxygen and nitrogen species ( R O S / R N S ROS/RNS ROS / RNS ), inducing cell membrane lipid peroxidation.

Neuroinflammation & Edema: Cytokines ( I L - 1 β IL\text{-}1\beta I L - 1 β , T N F - α TNF\text{-}\alpha TNF - α ) and microglial activation disrupt the blood-brain barrier ( B B B BBB BBB ), compounding cytotoxic cellular swelling with vasogenic edema and precipitating intracranial hypertension.

Brain Trauma Foundation Guidelines: ICP, CPP, and SBP Targets

The Brain Trauma Foundation ( B T F BTF BTF ) 4th Edition guidelines establish evidence-based resuscitation thresholds for severe TBI:

Parameter BTF 4th Edition Target Clinical Rationale

ICP Threshold Treat when I C P > 22 mmHg ICP > 22\text{ mmHg} I CP > 22 mmHg Sustained I C P > 22 mmHg ICP > 22\text{ mmHg} I CP > 22 mmHg is independently associated with herniation and increased mortality.

CPP Target Maintain C P P = 60 – 70 mmHg CPP = 60\text{--}70\text{ mmHg} CPP = 60 – 70 mmHg C P P < 60 mmHg CPP < 60\text{ mmHg} CPP < 60 mmHg causes secondary cerebral ischemia; targeting C P P > 70 mmHg CPP > 70\text{ mmHg} CPP > 70 mmHg with fluids/pressors increases the risk of A R D S ARDS A R D S five-fold.

Systolic Blood Pressure (SBP) ≥ 100 mmHg \ge 100\text{ mmHg} ≥ 100 mmHg (age 50 – 69 y 50\text{--}69\text{ y} 50 – 69 y );; ≥ 110 mmHg \ge 110\text{ mmHg} ≥ 110 mmHg (age 15 – 49 15\text{--}49 15 – 49 or ≥ 70 y \ge 70\text{ y} ≥ 70 y ) Age-stratified thresholds optimize cerebral perfusion; hypotension is the single most potent secondary predictor of poor neurological outcome.

Advanced Neuromonitoring Target P b t O 2 ≥ 20 mmHg PbtO_2 \ge 20\text{ mmHg} P b t O 2 ​ ≥ 20 mmHg Brain tissue oxygen tension < 15 mmHg < 15\text{ mmHg} < 15 mmHg denotes cellular hypoxia requiring augmented delivery or metabolic suppression.

Important

Calculate cerebral perfusion pressure as C P P = M A P − I C P CPP = MAP - ICP CPP = M A P − I CP . Level the arterial transducer at the external auditory meatus (foramen of Monro) rather than the right atrium to prevent overestimating cerebral perfusion when the head of the bed is elevated 30 ∘ 30^\circ 3 0 ∘ .

Traumatic Extra-Axial Hematomas & Surgical Evacuation Criteria

Standardized neurosurgical guidelines govern the operative management of traumatic intracranial collections:

Lesion Type Vascular Source & Imaging Hallmarks Emergent Surgical Indications

Epidural Hematoma (EDH) Middle meningeal artery/vein ( 85 % 85\% 85% ); pterion/temporal fracture; biconvex (lenticular) hyperdensity limited by cranial sutures Volume > 30 mL > 30\text{ mL} > 30 mL regardless of GCS score;; OR thickness > 15 mm > 15\text{ mm} > 15 mm , midline shift > 5 mm > 5\text{ mm} > 5 mm , or GCS drop ≥ 2 \ge 2 ≥ 2 in non-operative candidates

Acute Subdural Hematoma (ASDH) Parasagittal bridging cortical veins; cortical lacerations; crescentic hyperdensity crossing cranial sutures Thickness > 10 mm > 10\text{ mm} > 10 mm OR midline shift > 5 mm > 5\text{ mm} > 5 mm regardless of GCS;; OR GCS drop ≥ 2 \ge 2 ≥ 2 points, pupillary asymmetry, or I C P > 20 – 22 mmHg ICP > 20\text{--}22\text{ mmHg} I CP > 20 – 22 mmHg

Traumatic Contusions Coup/contrecoup impact against orbital roofs/sphenoid wings; inferior frontal & anterior temporal poles Volume > 50 mL > 50\text{ mL} > 50 mL , midline shift ≥ 5 mm \ge 5\text{ mm} ≥ 5 mm , cisternal effacement, or progressive neurological deterioration / refractory ICP

Clinical Nuances

Epidural Hematoma: An EDH collects between the inner skull table and periosteal dura. Classically, 20 – 30 % 20\text{--}30\% 20 – 30% exhibit a "lucid interval" —concussive loss of consciousness followed by temporary lucidity, then rapid uncal herniation (ipsilateral fixed, dilated pupil and contralateral hemiparesis). Evacuate if volume > 30 mL > 30\text{ mL} > 30 mL regardless of GCS.

Acute Subdural Hematoma: An ASDH collects beneath the visceral dura, tracking across sutures. ASDH is frequently associated with severe underlying parenchymal contusion and hemispheric edema, carrying 40 – 60 % 40\text{--}60\% 40 – 60% mortality. Evacuate if thickness > 10 mm > 10\text{ mm} > 10 mm or midline shift > 5 mm > 5\text{ mm} > 5 mm .

Contusions & "Blossoming": Contusions occur where brain tissue impacts irregular skull base surfaces. They routinely expand— "blossoming" —over the first 24 to 72 hours due to coalescing petechial hemorrhages and edema. Surveillance head CT within 12 to 24 hours (or immediately upon decline) is mandatory.

Diffuse Axonal Injury: Biomechanics, Grading, and Neuroimaging

Diffuse axonal injury ( D A I DAI D A I ) occurs when rotational acceleration-deceleration forces create dynamic shear strains across tissues of differing densities (gray-white junction). Dynamic membrane stretch disrupts axolemmal permeability, provoking calcium influx, calpain activation, and neurofilament compaction. Swollen axonal varicosities and retraction balls form over 24 to 48 hours, culminating in secondary axotomy and wallerian degeneration.

Adams Histopathological Classification

Grade I: Axonal injury confined to lobar white matter (parasagittal gray-white junction, frontal/temporal lobes).

Grade II: Axonal injury involving lobar white matter PLUS the corpus callosum (predominantly the splenium ).

Grade III: Axonal injury involving lobar white matter, corpus callosum, PLUS the dorsolateral rostral brainstem (superior cerebellar peduncles, midbrain tegmentum).

Non-contrast CT is insensitive to DAI, often appearing normal or showing only subtle punctate petechiae ( < 5 mm < 5\text{ mm} < 5 mm ). MRI with Susceptibility-Weighted Imaging (SWI) or gradient-recalled echo ( G R E GRE GRE ) is diagnostic, revealing innumerable hypointense "blooming" microhemorrhages in the callosum and brainstem. Clinically, DAI produces prolonged post-traumatic coma disproportionate to initial CT findings.

Post-Traumatic Seizure Prophylaxis Protocols

Seizures after TBI are categorized by onset timing:

Early Post-Traumatic Seizures (PTS): Occur within 7 days of injury, provoked by acute cortical contusions, blood products, and metabolic derangements.

Late Post-Traumatic Epilepsy (PTE): Occur after 7 days, reflecting chronic gliotic scaring and epileptogenic network remodeling.

Note

The BTF guidelines recommend a 7-day course of prophylactic antiseizure medication (ASM) —using either levetiracetam or phenytoin —to suppress early PTS in severe TBI. However, prophylaxis does NOT reduce late post-traumatic epilepsy or improve overall survival. Prophylactic ASMs should be discontinued on post-injury day 7 if no clinical or electrographic seizures have occurred, preventing cognitive slowing, cytopenias, and unnecessary drug toxicity.