Epidemiology
- Traumatic Brain Injury (TBI) is the Leading Cause of Death for Patients Age 1-45 y/o in North America [MEDLINE]
- Many Survivors Have Significant Disability
Physiology
Primary Brain Injury
- General Comments: primary brain injury occurs at the time of trauma
- Mechanisms of Primary Brain Injury
- Diffuse Axonal Injury Due to Shearing: usually involves the hemispheric gray-white matter junction, corpus callosum, and/or midbrain
- Usually present with coma without an increase in intracranial pressure
- Focal Cerebral Contusion: common in basal frontal and temporal regions (due to susceptibility to direct impact on the basal skull surface during acceleration/deceleration injuries)
- These are the most frequently observed lesions
- Intraparenchymal hematoma may occur from coalescence of cerebral contusions or disruption of intraparenchymal blood vessels
- Extra-Axial Hematoma
- Epidural Hematoma (see Epidural Hematoma, [[Epidural Hematoma]]): due to tear in dural vessels (middle meningeal artery, etc)
- Almost always associated with skull fracture
- Tend to not be associated with underlying parenchymal brain injury
- Intraventricular Hemorrhage: due to tearing of subependymal veins, extension from adjacent intraparenchymal hemorrhage, or extension from subarachnoid hemorrhage
- Subarachnoid Hemorrhage (SAH) (see Subarachnoid Hemorrhage, [[Subarachnoid Hemorrhage]]): due to disruption of small pial vessels, extension from intraventricular hemorrhage, or extension from superficial parenchymal hemorrhage
- Tend to occur in the sylvian fissures and interpeduncular cisterns
- Subdural Hematoma (SDH) (see Subdural Hematoma, [[Subdural Hematoma]]): due to damage to bridging veins (which drain cerebral cortical surfaces to dural venous sinuses) or from extension from superficial cortical contusions
- Tend to be associated with underlying parenchymal brain injury
- Epidural Hematoma (see Epidural Hematoma, [[Epidural Hematoma]]): due to tear in dural vessels (middle meningeal artery, etc)
- Diffuse Axonal Injury Due to Shearing: usually involves the hemispheric gray-white matter junction, corpus callosum, and/or midbrain
Secondary Brain Injury
- General Comments: secondary brain injury occurs subsequent to the initial trauma and continues for hours-days
- Mechanisms of Secondary Brain Injury
- Apoptosis
- Electrolyte Imbalance
- Inflammatory Response
- Mitochondrial Dysfunction
- Neurotransmitter-Mediated Excitotoxicity Resulting in Glutamate, Free-Radical Injury to Cell Membranes
- Secondary Brain Ischemia Resulting from Vasospasm, Focal Microvascular Occlusion, and Vascular Injury
Other Aspects
- Impaired Cerebral Autoregulation
- Normally, Via Autoregulation, the Brain Maintains an Adequate Cerebral Blood Flow Across a Wide Range of Mean Arterial Blood Pressures (MAP) From 50-100 Meg Hg
- In TBI, Cerebral Autoregulation is Impaired in Approximately 33% of TBI Cases: resulting in the brain demonstrating “pressure-passive” hemodynamics
- Increased MAP (hypertension) may then result in increased cerebral blood flow and hypermedia, resulting in elevated intracranial pressure (ICP)
- Decreased MAP (hypotension) may result in brain hypoperfusion and ischemia
Diagnosis
Head CT (see Head Computed Tomography, [[Head Computed Tomography]])
- xxx
Brain MRI (see Brain Magnetic Resonance Imaging, [[Brain Magnetic Resonance Imaging]])
- xxx
External Ventricular Drain (EVD) (see External Ventricular Drain, [[External Ventricular Drain]])
- Indications for Monitoring in the Setting of Traumatic Brain Injury
- Survivable Severe TBI with Associated Abnormalities on Head CT at Time of Admission
- TBI in Patient Age >40 y/o with Hypotension or Abnormal Flexion/Extension in Response to Pain with Normal Head CT at Time of Admission
- Contraindications
- Coagulopathy (see Coagulopathy, [[Coagulopathy]]): relative contraindication
- Thrombocytopenia with Platelets <100k (see Thrombocytopenia, [[Thrombocytopenia]]): relative contraindication
- Adverse Effects/Complications
- Intracerebral Hemorrhage: rate of hemorrhage with ventricular catheter is 1-7%
- Rate of Hemorrhage for Intraparenchymal Monitor is Less Than That of Ventricular Catheter
- Hemorrhages Rarely Require Surgical Evacuation
- Infection/Ventriculitis (see Central Nervous System Device Infection, [[Central Nervous System Device Infection]])
- Culture of Tip of External Ventricular Drains May Demonstrate Bacterial Colonization: however, the rate of invasive infection is lower
- Risk of Infection is Higher with Ventricular Catheter (1-27%) Than with Parenchymal Monitor
- Risk Factors for Infection
- Leakage Around the Ventriculostomy Site
- Longer Duration of Catheter Placement
- Presence of Open Skull Fracture with Leakage of Cerebrospinal Fluid
- Intracerebral Hemorrhage: rate of hemorrhage with ventricular catheter is 1-7%
Glasgow Coma Scale (GCS)
- Eye Opening
- Spontaneous: 4
- Response to Verbal Command: 3
- Response to Pain: 2
- No Eye Opening: 1
- Best Verbal Reponse
- Oriented: 5
- Confused: 4
- Inappropriate Words: 3
- Incomprehensible Sounds: 2
- No Verbal Response: 1
- Best Motor Response
- Obeys Commands: 6
- Localizing Response to Pain: 5
- Withdrawal Response to Pain: 4
- Flexion to Pain: 3
- Extension to Pain: 2
- No Motor Response: 1
- Total
- Range: 3-15 (3 is the worst and 15 is the best)
- Score 13+: mild brain injury
- Score 9-12: moderate brain injury
- Score 8 or Less: severe brain injury
Clinical Manifestations
Hematologic Manifestations
- Coagulopathy (see Coagulopathy, [[Coagulopathy]])
- Epidemiology: approximately 33% of TBI patients develop coagulopathy -> this is associated with increased risk of hemorrhage, poor neurologic outcome, and increased mortality rate
- Physiology: systemic release of tissue factor and brain phospholipid -> Intravascular coagulation and consumptive coagulopathy
Neurologic Manifestations
Anxiety/Depression (see Anxiety, [[Anxiety]] and Depression, [[Depression]])
- Epidemiology: high rates are noted following TBI
Chronic Pain
- Epidemiology: common following TBI
- May Further Exacerbate Sleep Disturbances
Coma (see Obtundation-Coma, [[Obtundation-Coma]])
- Epidemiology: xxx
Increased Intracranial Pressure (see Increased Intracranial Pressure, [[Increased Intracranial Pressure]])
- xxxx
Post-Traumatic Stress Disorder (PTSD) (see Post-Traumatic Stress Disorder, [[Post-Traumatic Stress Disorder]])
- Epidemiology: common (especially in military populations) following TBI
Seizures (see Seizures, [[Seizures]])
- Epidemiology
- Incidence of Seizures Within the First 1-2 Weeks: 6-10% (although may be as high as 30%)
- Incidence of Non-Convulsive Seizures: 15-25% in patients with TBI and coma
Sleep-Wake Disturbances
- Epidemiology: prevalent and persistent following TBI
- Clinical: may occur acutely or chronically following TBI of any severity
- Difficulty Maintaining Sleep
- Early Morning Awakenings
- Excessive Daytime Somnolence (see Excessive Daytime Somnolence, [[Excessive Daytime Somnolence]])
- Increased Need for Sleep
- Insomnia (se Insomnia, [[Insomnia]])
- Nightmares (see Nightmares, [[Nightmares]])
- Sleep Fragmentation
Pulmonary Manifestations
Aspiration Pneumonia (see Aspiration Pneumonia, [[Aspiration Pneumonia]])
- Epidemiology
Increased Risk for Obstructive Sleep Apnea (OSA)/Central Sleep Apnea (CSA)
- Epidemiology: prevalence of obstructive sleep apnea was 23% following TBI [MEDLINE]
Other Manifestations
- xxxx
Treatment
General Measures
- Correction of Electrolyte Imbalances: when present
- Care in Specialized Trauma Center: associated with improved outcome
- Study of the Impact of High-Volume Trauma Centers on Outcome After TBI (J Trauma Acute Care Surg, 2013) [MEDLINE]
Deep Venous Thrombosis (DVT) Prophylaxis (see Deep Venous Thrombosis, [[Deep Venous Thrombosis]])
- Measures
- Sequential Compression Devices (SCD’s)
- Pharmacologic Prophylaxis
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Graduated Compression Stockings/Sequential Compression Device (SCD’s) are Recommended (Level III Recommendation): continue use until patient is ambulatory
- Low Molecular Weight Heparin or Low Dose Unfractionated Heparin Should Be Used in Combination with Mechanical Prophyaxis (Level III Recommendation): however, there is an increased risk of expansion of intracranial hemorrhage
- Insufficient Evidence to Determine the Preferred Agent, Dose, or Timing of Pharmacologic DVT Prophylaxis
Hemodynamic Management
- Rationale: hypotension causes cerebral vasodilation
- Hemodynamic Monitoring
- Monitor Central Venous Pressure (CVP): to maintain adequate fluid status
- Clinical Efficacy
- SAFE Study: Comparing Crystalloid (Normal Saline) vs Colloid (4% Albumin) in Heterogenous Population of ICU Patients (2004) [MEDLINE]: colloid (albumin) use in the subgroup of patients with TBI resulted in a higher mortality rate
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Hypotension <90 mm Hg Should Be Avoided (Level II Recommendation)
Hemostatic Therapy
- Recommendations
- Management of Non-Coagulopathic Patients: hemostatic therapy is not indicated
- Management of Elevated INR (Unrelated to Coumadin): maintain INR <1.4 with FFP, prothrombin complex concentrate, etc
- Role of Recombinant Factor VIIa (NovoSeven RT) (see Factor VIIa, [[Factor VIIa]])
- FVIIa Traumatic ICH Study Group Prospective Trial in TBI (Neurosurgery, 2008) [MEDLINE]: recombinant factor VIIa decreased hematoma progression, but did not decrease the mortality rate (but there was a trend toward increased rate of DVT’s at day 3)
- Role of Recombinant Factor VIIa (NovoSeven RT) (see Factor VIIa, [[Factor VIIa]])
- Management of Coumadin Anticoagulation (If Present): maintain INR <1.4
- Fresh Frozen Plasma (FFP) (see Fresh Frozen Plasma, [[Fresh Frozen Plasma]])
- Prothrombin Complex Concentrate-4 Factor (Kcentra, Beriplex, Confidex) (see Prothrombin Complex Concentrate-4 Factor, [[Prothrombin Complex Concentrate-4 Factor]])
- Vitamin K (see Vitamin K, [[Vitamin K]])
- Management of Platelet Dysfunction (Drug-Induced, etc)
- Systematic Review of Platelet Transfusion in TBI in Patients on Pre-Injury Antiplatelet Therapy (J Trauma Acute Care Surg, 2012) [MEDLINE]: platelet transfusion in this setting is of unclear benefit (due to poor quality data)
- Management of Thrombocytopenia (If Present): maintain platelet count >75k
Infection Prophylaxis
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Peri-Procedural Antibiotics are Recommended for Intubation to Decrease the Risk of Pneumonia (Level II Recommendation): however, these do not decrease length of stay or mortality rate
- Early Tracheostomy Should Be Performed to Decrease Ventilator Days (see Tracheostomy, [[Tracheostomy]]): however, it does not decrease mortality rate or rate of pneumonia
- Routine Ventricular Catheter Exchange to Prevent Infection is Not Recommended (Level III Recommendation)
- Prophylactic Antibiotics to Prevent Ventricular Catheter Infection are Not Recommended (Level III Recommendation)
- Early Extubation in Qualified Patients Can Be Done Without an Increased Risk of Pneumonia (Level III Recommendation)
Management of Increased Intracranial Pressure (see Increased Intracranial Pressure, [[Increased Intracranial Pressure]])
Analgesia
- Agents
- Fentanyl (Sublimaze) (see Fentanyl, [[Fentanyl]])
- Morphine (see Morphine, [[Morphine]])
- Sufentanil (Sufenta) (see Sufentanil, [[Sufentanil]])
Central Venous Pressure (CVP) Monitoring (see Hemodynamics, [[Hemodynamics]])
- Recommendations
- Avoid Hypervolemia
Corticosteroids (see Corticosteroids, [[Corticosteroids]])
- Clinical Efficacy
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Corticosteroids are Not Recommended to Decrease Intracranial Pressure: high dose methylprednisolone is associated with increased mortality in moderate-severe TBI
Decompressive Craniectomy (see Decompressive Craniectomy, [[Decompressive Craniectomy]])
- Procedure: removal of part of skull may be done solely to decrease the intracranial pressure or as part of an evacuation procedure
- Clinical Efficacy: clinical benefit in TBI is unclear, further study is required
- DECRA Trial (NEJM, 2011) [MEDLINE]
- Bifrontotemporoparietal Decompressive Craniectomy in Adults with TBI and Refractory Increased ICP Decreased ICP and Length of ICU Stay, But was Associated with No Impact on Mortality and a Higher Number of Unfavorable Outcomes
- Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure (RESCUEicp) Study: results pending
- DECRA Trial (NEJM, 2011) [MEDLINE]
- Complications
- Infection
Elevation of Head of to Bed to 30 Degrees
- Standard Therapy
Hypertonic Saline (see Hypertonic Saline, [[Hypertonic Saline]])
- Pharmacology: probably induces osmotic mobilization of water across the intact blood-brain barrier, decreasing cerebral water content
- Adverse Effects
- Fluid Overload (Due to Sodium Load)
- Hypernatremia (see Hypernatremia, [[Hypernatremia]])
- Clinical Efficacy
- Comparison of Mannitol with 23.4% Hypertonic Saline in Decreasing Intracranial Pressure in TBI (Neurosurgery, 2005) [MEDLINE]
- No Difference Between Mannitol and Hypertonic Saline (23.4%) in Decreasing in ICP in TBI: however, duration of hypertonic saline effect (96 min) was longer than that of mannitol (59 min)
- Systematic Review and Meta-Analysis of Hypertonic Saline (Crit Care Med, 2013) [MEDLINE]
- Hypertonic Saline (23.4%) Decreased Intracranial Pressure by 50% within 60 min in TBI
- Comparison of Mannitol with 23.4% Hypertonic Saline in Decreasing Intracranial Pressure in TBI (Neurosurgery, 2005) [MEDLINE]
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Insufficient Evidence to Make Recommendation for Use of Hypertonic Saline
Hyperventilation
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Prophylactic Hyperventilation (pCO2 <25 mm Hg) is Not Recommended (Level II Recommendation)
- Hyperventilation is Recommended as a Temporizing Measure to Decrease an Elevated Intracranial Pressure (Level III Recommendation)
- However, Hyperventilation Should be Avoided During the First 24 hrs After Injury: during this period, cerebral blood flow is often critically decreased
- If Hyperventilation is Used, Jugular Venous Oxygen Saturation (SjO2) or Brain Tissue Oxygenation are Recommended to Monitor Therapy
Intracranial Pressure (ICP) Monitoring (see Increased Intracranial Pressure, [[Increased Intracranial Pressure]])
- Rationale
- Cerebral Perfusion Pressure is a Surrogate for Cerebral Blood Flow
- Cerebral Perfusion Pressure (CPP) = MAP – ICP
- Episodes of Hypotension, Increased ICP, and Low CPP are Associated with Secondary Brain Injury and Worse Outcome (J Neurosurg, 2002) [MEDLINE]
- Allows Drainage of Cerebrospinal Fluid from Ventricle: when using an external ventricular drain
- Indications (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- All Salvageable Patients with Severe TBI, GCS 3-8 After Resuscitation, and an Abnormal CT Scan (Hematoma, Contusion, Edema, Herniation, Compressed Basal Cisterns) (Level II Recommendation)
- Severe TBI with Normal CT Scan with Two or More Criteria at Admission: Age >40 y/o, Unilateral or Bilateral Motor Posturing, SBP <90 mm Hg (Level III Recommendation)
- Contraindications
- Coagulopathy Which Cannot Be Corrected (see Coagulopathy, [[Coagulopathy]])
- Infection Preventing Insertion
- Device
- External Ventricular Drain (EVD) (see External Ventricular Drain, [[External Ventricular Drain]])
- Complications
- Intracerebral Hemorrhage: rate of hemorrhage with ventricular catheter is 1-7%
- Rate of Hemorrhage for Intraparenchymal Monitor is Less Than That of Ventricular Catheter
- Hemorrhages Rarely Require Surgical Evacuation
- Infection/Ventriculitis (see Ventriculitis, [[Ventriculitis]])
- Culture of Tip of External Ventricular Drains May Demonstrate Bacterial Colonization: however, the rate of invasive infection is lower
- Risk of Infection is Higher with Ventricular Catheter (1-27%) Than with Parenchymal Monitor
- Risk Factors for Infection
- Leakage Around the Ventriculostomy Site
- Longer Duration of Catheter Placement
- Presence of Open Skull Fracture with Leakage of Cerebrospinal Fluid
- Intracerebral Hemorrhage: rate of hemorrhage with ventricular catheter is 1-7%
- Clinical Efficacy
- Trial of Intracranial Pressure Monitoring in TBI (NEJM, 2012) [MEDLINE]
- Maintaining ICP <20 mm Hg Did Not Improve Outcome (Based on Functional and Cognitive Status), 6-Month Mortality Rate, or Median Length of ICU Stay, as Compared to Clinical Exam/Imaging-Based Management
- Trial of Intracranial Pressure Monitoring in TBI (NEJM, 2012) [MEDLINE]
- Recommendations for Intracranial Pressure Thresholds (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Treatment Should Be Initiated for ICP >20 mm Hg (Level II Recommendation)
- Combination of ICP + Clinical Findings + Brain Findings Should Be Used to Determine the Need for Treatment of ICP (Level III Recommendation)
- Recommendations for Cerebral Perfusion Pressure Thresholds (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]: target CPP 50-70 mm Hg (patients with intact cerebral autoregulation will tolerate higher CPP values)
- Maintenance of Cerebral Perfusion Pressure >70 mm Hg with Fluids/Pressors Should Be Avoided Due to Risk of ARDS (Level II Recommendation): excessive hypervolemia should be avoided
- Cerebral Perfusion Pressure <50 mm Hg Should Be Avoided (Level III Recommendation)
Mannitol (see Mannitol, [[Mannitol]])
- Indications
- Increased Intracranial Pressure (see Increased Intracranial Pressure, [[Increased Intracranial Pressure]])
- Pharmacology: osmotic diuretic
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Mannitol (Dose: 0.25-1.00 g/kg) is Effective to Control Increased Intracranial Pressure (Level II Recommendation)
- Hypotension (SBP <90 mm Hg) Should Be Avoided
- Restrict Mannitol Use Prior to Intracranial Pressure Monitoring to Patients with Transtentorial Herniation or Progressive Neurologic Deterioration Not Attributable to an Extracranial Etiology (Level III Recommendation)
- Mannitol (Dose: 0.25-1.00 g/kg) is Effective to Control Increased Intracranial Pressure (Level II Recommendation)
Optimization of Cerebral Venous Drainage
- Procedure
- Loosen Neck Braces (If Too Tight)
- Maintain Neck in Neutral Position
Sedation (see Sedation, [[Sedation]])
- Agents
- Barbiturates (see Barbiturates, [[Barbiturates]])
- Pharmacology: decrease cerebral metabolism and cerebral blood flow (decreasing intracranial pressure)
- Pentobarbital (see Pentobarbital, [[Pentobarbital]])
- Dexmedetomidine (Precedex) (see Dexmedetomidine, [[Dexmedetomidine]])
- Properties
- Analgesic Effect
- Anxiolytic Effect
- Decreases Intracranial Pressure
- Sedative Effect
- Sympatholytic Effect
- No Effect on Seizure Threshold
- No Significant Respiratory Depression
- Properties
- Midazolam (Versed) (see Midazolam, [[Midazolam]])
- Propofol (Diprivan) (see Propofol, [[Propofol]])
- Properties
- Amnestic Effect (see Amnesia, [[Amnesia]])
- Anti-Emetic Effect
- Anxiolytic Effect
- Decreases Intracranial Pressure (see Increased Intracranial Pressure, [[Increased Intracranial Pressure]])
- Increases Seizure Threshold
- Sedative Effect
- No Analgesic Effect
- Large Lipid Load: requiring adjustment of enteral/parenteral nutritional support
- Properties
- Barbiturates (see Barbiturates, [[Barbiturates]])
- Clinical Efficacy
- Systematic Review of Sedatives in TBI (Crit Care MED, 2011) [MEDLINE]
- No Evidence that Any Sedative is Superior to Another in TBI in Terms of Patient-Centered Outcomes, Intracranial Pressure, or Cerebral Perfusion Pressure
- High Bolus Doses of Opiates Have Potentially Deleterious Effects on Intracranial Pressure and Cerebral Perfusion Pressure
- Systematic Review of Sedatives in TBI (Crit Care MED, 2011) [MEDLINE]
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Propofol is Recommended for Increased Intracranial Pressure: however, propofol has not been shown to improve mortality or 6-mo outcome (in addition, high dose propofol can produce significant morbidity)
- Barbiturates are Recommended for Increased Intracranial Pressure Refractory to Other Medical/Surgical Therapies
- Pentobarbital (see Pentobarbital, [[Pentobarbital]])
Therapeutic Hypothermia (see Therapeutic Hypothermia, [[Therapeutic Hypothermia]])
- Rationale: therapeutic hypothermia lowers intracranial pressure
- See Below Under “Management of Body Temperature”
Treatment of Fever (see Fever, [[Fever]])
- Rationale: fever causes cerebral vasodilation
- See Below Under “Management of Body Temperature”
Treatment of Hyponatremia (see Hyponatremia, [[Hyponatremia]])
- Rationale: hyponatremia causes cerebral edema
- Standard Therapy
Management of Seizures (see Seizures, [[Seizures]])
- Rationale: seizures cause cerebral vasodilation
- Agents
- Benzodiazepines (see Benzodiazepines, [[Benzodiazepines]]): increase seizure threshold
- Lorazepam (Ativan) (see Lorazepam, [[Lorazepam]])
- Propofol (Diprivan) (see Propofol, [[Propofol]]): increases seizure threshold
- Benzodiazepines (see Benzodiazepines, [[Benzodiazepines]]): increase seizure threshold
- Clinical Efficacy
- Systematic Review of Anti-Epileptic Drugs for Seizures Following TBI (Cochrane Database Syst Rev, 2001) [MEDLINE]
- Prophylactic Anti-Epileptics are Effective in Decreasing Early Seizures
- Prophylactic Anti-Epileptics Do Not Decrease the Occurrence of Late Seizures or Impact Neurologic Disability or Mortality Rate
- Systematic Review of Anti-Epileptic Drugs for Seizures Following TBI (Cochrane Database Syst Rev, 2001) [MEDLINE]
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Anticonvulsants are Recommended to Decrease the Incidence of Early Post-Traumatic Seizures (Within 7 Days of Injury): however, post-traumatic seizures are not associated with worse outcomes
- Prophylactic Phenytoin/Valproic Acid is Not Recommended to Prevent Late Post-Traumatic Seizures (Level II Recommendation)
Management of Serum Glucose
- Clinical Efficacy
- Study of Hyperglycemia in Traumatic Brain Injury (J Trauma, 2005) [MEDLINE]: early hyperglycemia is associated with poor outcome in severe TBI
- Recommendations
- Maintain Normoglycemia
Management of Body Temperature
Treatment of Fever (see Fever, [[Fever]])
- Clinical Efficacy
- Study of Predictors of Mortality in TBI (J Neurosurgery, 2002) [MEDLINE]: fever predicts poor outcome in TBI
- Recommendations
- Maintain Normothermia
- Techniques
- Anti-Pyretics
- Endovascular Temperature Management Catheters
- Surface Cooling Blankets
Therapeutic Hypothermia (see Therapeutic Hypothermia, [[Therapeutic Hypothermia]])
- Rationale: therapeutic hypothermia lowers intracranial pressure
- Clinical Efficacy
- Cochrane Database Systematic Review of Therapeutic Hypothermia in Traumatic Brain Injury (Cochrane Database Syst Rev, 2009) [MEDLINE]: therapeutic hypothermia may be effective in reducing death and unfavourable outcomes for traumatic head injured patients, but significant benefit was found only in the low quality trials -> therapeutic hypothermia is not recommended in traumatic brain injury
- Systematic Review of Therapeutic Hypothermia in Traumatic Brain Injury (CJEM, 2010) [MEDLINE]: prophylactic mild-to-moderate therapeutic hypothermia (32-34 degrees C) in traumatic brain injury (Glasgow coma scale score < or = 8) decreased mortality and improved rates of good neurologic recovery
- Maximal benefit occurred with cooling continued for at least 72 hours and/or until stable normalization of intracranial pressure for at least 24 hrs
- National Acute Brain Injury Study: Hypothermia II Trial (Lancet, 2011) [MEDLINE]: therapeutic hypothermia to 33 or 35 degrees C (in patients enrolled within 2.5 hrs of injury) had no clinical benefit in terms of Glasgow outcome scale score at 6 mo
- Greater benefit from therapeutic hypothermia was observed in patients undergoing surgical removal of hematomas, as compared with those with diffuse axonal/brain injury
- Systematic Review of Therapeutic Hypothermia in Traumatic Brain Injury (Brain Injury, 2012) [MEDLINE]: therapeutic hypothermia decreased intracranial pressure
- Adverse Effects
- Rewarming Can Increase Intracranial Pressure
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Prophylactic Therapeutic Hypothermia is Not Associated with Decreased Mortality in Traumatic Brain Injury (When Compared to Normothermic Controls) (Level III Recommendation)
- However, When Maintained for >48 hrs, Mortality May Be Decreased
- Prophylactic Therapeutic Hypothermia is Associated with Significantly Higher GCS Scores (When Compared to Normothermic Controls)
- Prophylactic Therapeutic Hypothermia is Not Associated with Decreased Mortality in Traumatic Brain Injury (When Compared to Normothermic Controls) (Level III Recommendation)
- Recommendations
- Therapeutic Hypothermia Has Unclear Clinical Benefit in TBI: however, may be considered in patients with refractory elevations in intracranial pressure, despite other therapy
Nutrition
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Patients Should Be Fed to Attain Full Caloric Replacement by Day 7 Post-Injury
Renal Management
- Choice of Intermittent Hemodialysis vs Continuous Venovenous Hemodialysis (CVVHD)
- If Hemodialysis is Required, CVVHD is Preferred Over Intermittent HD, Due to Rapid Solute Changes and Potential for Hypotension with Intermittent HD (Which May Exacerbate Cerebral Ischemia) (see Hemodialysis, [[Hemodialysis]])
Respiratory Management
- Indications for Intubation/Mechanical Ventilation
- Glasgow Coma Scale Score <8: early intubation is recommended, if prehospital expertise is available
- Respiratory Failure (see Respiratory Failure, [[Respiratory Failure]])
- Type I Hypoxemic Respiratory Failure
- Type II Ventilatory/Hypercapnic Hypoxemic Respiratory Failure
- Strategies for Mechanical Ventilation (see xxxx, [[xxxx]])
- Avoid Coughing (see Cough, [[Cough]]): generally achieved using sedation, clearance of airway obstruction, etc
- Avoid Hypoxemia (see Hypoxemia, [[Hypoxemia]]): hypoxemia causes cerebral vasodilation
- Avoid Hypercapnia (see Hypercapnia, [[Hypercapnia]]): hypercapnia causes cerebral vasodilation
- Patient-Ventilator Dyssynchrony: dyssynchrony increases venous pressure
- Recommendations (Guidelines for the Management of Severe Traumatic Brain Injury, 2007) [MEDLINE]
- Avoid Hypotension <90 mm Hg (Level II Recommendation)
- Avoid Hypoxemia (pO2 <60 mm Hg or SaO2 <90%) (Level III Recommendation)
Surgical Management
Epidural Hematoma (see Epidural Hematoma, [[Epidural Hematoma]])
- xxx
Subdural Hematoma (see Subdural Hematoma, [[Subdural Hematoma]])
- xxx
Intracerebral Hemorrhage (see Intracerebral Hemorrhage, [[Intracerebral Hemorrhage]])
- xxx
Penetrating Brain Injury
- xxx
Depressed Skull Fracture
- xxx
XXX
- xxx
Prognosis
- Prognostic Factors in TBI [MEDLINE]
- Glasgow Coma Score
- Age
- Pupillary Response/Size
- Hypoxia
- Hyperthermia
- Increased Intracranial Pressure
- Outcome After 1 Year in TBI [MEDLINE]
- Good Recovery: 31.56%
- Moderate Disability: 14.07%
- Severe Disability: 24.35%
- Vegetative State: 0.59%
- Death: 29.43%
References
General
- Early indicators of prognosis in 846 cases of severe traumatic brain injury. J Neurotrauma 2002;19(7):869-874. doi: 10.1089/08977150260190456 [MEDLINE]
- Predicting recovery in patients suffering from traumatic brain injury by using admission variables and physiological data: a comparison between decision tree analysis and logistic regression. J Neurosurg. 2002;97(2):326 [MEDLINE]
- Early management of severe traumatic brain injury. Lancet. 2012 Sep;380(9847):1088-98 [MEDLINE]
Treatment
General
- Guidelines for the management of severe traumatic brain injury. J Neurotrauma. 2007;24 Suppl 1:S1-106 [MEDLINE]
- Guidelines for the management of severe traumatic brain injury. Editor’s commentary. J Neurotrauma 2007; 24 Suppl 1:2 p preceding S1 [MEDLINE]
- Prevalence and consequences of sleep disorders in traumatic brain injury. J Clin Sleep Med. 2007 Jun;3(4):349-56 [MEDLINE]
- Traumatic brain injury: intensive care management. Br J Anaesth 2007;99:32–42 [MEDLINE]
- Mortality reduction after implementing a clinical practice guidelines-based management protocol for severe traumatic brain injury. J Crit Care 2010; 25:190-195 [MEDLINE]
- A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med 2012;367:2471–2481 [MEDLINE]
- Critical care management of severe traumatic brain injury in adults. Scand J Trauma Resusc Emerg Med 2012; 20:12 [MEDLINE]
- Early management of severe traumatic brain injury. Lancet. 2012 Sep;380(9847):1088-98 [MEDLINE]
- High-volume trauma centers have better outcomes treating traumatic brain injury. J Trauma Acute Care Surg. 2013 Jan;74(1):143-7; discussion 147-8 [MEDLINE]
Sedation
- High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg. 1988 Jul;69(1):15-23 [MEDLINE]
- Sedation for critically ill adults with severe traumatic brain injury: a systematic review of randomized controlled trials. Crit Care Med. 2011;39:2743–2751 [MEDLINE]
- Sedation in traumatic brain injury. Emerg Med Int. 2012; vol 2012; article ID 637171, pp 1–11 [MEDLINE]
Hemodynamic Management
- SAFE Study. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350:2247–2256 [MEDLINE]
Hemostatic Therapy
- rFVIIa Traumatic ICH Study Group. Recombinant factor VIIA in traumatic intracerebral hemorrhage: results of a dose-escalation clinical trial. Neurosurgery. 2008 Apr;62(4):776-86; discussion 786-8 [MEDLINE]
- Utility of platelet transfusion in adult patients with traumatic intracranial hemorrhage and preinjury antiplatelet use: a systematic review. J Trauma Acute Care Surg. 2012 Jun;72(6):1658-63 [MEDLINE]
Corticosteroids
- Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet. 2004;364(9442):1321 [MEDLINE]
- Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet. 2005;365(9475):1957 [MEDLINE]
Management of Increased Intracranial Pressure
- Hypertonic saline resuscitation of patients with head injury: a prospective, randomized clinical trial. J Trauma. 1998;44(1):50 [MEDLINE]
- Effects of 23.4% sodium chloride solution in reducing intracranial pressure in patients with traumatic brain injury: a preliminary study. Neurosurgery. 2005;57(4):727 [MEDLINE]
- Refractory intracranial hypertension and “second-tier” therapies in traumatic brain injury. Intensive Care Med. 2008;34:461–467 [MEDLINE]
- Sedation for critically ill adults with severe traumatic brain injury: a systematic review of randomized controlled trials. Crit Care Med. 2011 Dec;39(12):2743-51 [MEDLINE]
- Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364(16):1493 [MEDLINE]
- Hyperosmolar therapy for raised intracranial pressure. N Engl J Med. 2012;367:746–752 [MEDLINE]
- Traumatic intracranial hypertension. N Engl J Med. 2014;370:2121–2130. doi: 10.1056/NEJMra1208708 [MEDLINE]
- High-osmolarity saline in neurocritical care: systematic review and meta-analysis. Crit Care Med 2013;41:1353–1360. doi: 10.1097/CCM.0b013e31827ca4b3 [MEDLINE]
Management of Seizures
- Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev. 2001;(4):CD000173 [MEDLINE]
Management of Serum Glucose
- Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg. 1991;75(4):545 [MEDLINE]
- The influence of hyperglycemia on neurological outcome in patients with severe head injury. Neurosurgery. 2000;46(2):335 [MEDLINE]
- The impact of hyperglycemia on patients with severe brain injury. J Trauma. 2005;58(1):47 [MEDLINE]
Management of Body Temperature
- Predicting recovery in patients suffering from traumatic brain injury by using admission variables and physiological data: a comparison between decision tree analysis and logistic regression. J Neurosurg. 2002;97(2):326 [MEDLINE]
Therapeutic Hypothermia
- Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med 2001;344:556 [MEDLINE]
- Induced hypothermia and fever control for prevention and treatment of neurological injuries. Lancet 2008;371:1955 [MEDLINE]
- Hypothermia for traumatic head injury. Cochrane Database of Systematic Reviews 2009, Issue 2. Art. No.: CD001048. DOI: 10.1002/ 14651858.CD001048.pub4 [MEDLINE]
- Prophylactic hypothermia for traumatic brain injury: a quantitative systematic review. CJEM 2010; 12:355-364 [MEDLINE]
- Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial. Lancet Neurol 2011; 10:131-139 [MEDLINE]
- Therapeutic hypothermia for the management of intracranial hypertension in severe traumatic brain injury: a systematic review. Brain Inj 2012; 26:899-908 [MEDLINE]
- Therapeutic hypothermia for acute brain injuries. Scand J Trauma Resusc Emerg Med. 2015 Jun 5;23:42. doi: 10.1186/s13049-015-0121-3 [MEDLINE]