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Symptom
dx.
Clinical Reference
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ECG
Interpretation guide
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ECG
Interpretation guide
POCUS
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Diffuse Axonal Injury (Severe)
Cardiovascular Presentations
Abdominal aortic aneurysm
Acute coronary syndrome (NSTEMI)
Acute coronary syndrome (STEMI)
Acute decompensated heart failure
Acute limb ischemia
Acute mesenteric ischemia
Aortic dissection
Aortic stenosis
Atrial fibrillation and flutter
Bradyarrhythmia and heart block
Cardiac arrest
Deep vein thrombosis
Myocarditis
Pericarditis
Pulmonary embolism
Stable angina
Superficial thrombophlebitis
Superior vena cava syndrome
Supraventricular tachycardia
Syncope (cardiogenic)
Unstable angina
Ventricular tachycardia
Respiratory Presentations
Acute bronchitis
Acute respiratory failure
Aspiration pneumonia
Asthma exacerbation
Bronchiolitis
Community-acquired pneumonia
COVID-19 pneumonia
COPD exacerbation
Croup
Croup (laryngotracheobronchitis)
Epiglottitis
Hemothorax
Hospital-acquired pneumonia
Pleural effusion
Pneumothorax (traumatic)
Pulmonary contusion
Spontaneous pneumothorax
Neurological Presentations
Bell's palsy
Benign paroxysmal positional vertigo
Brain abscess
Cauda equina syndrome
Cervical radiculopathy
Concussion (mild traumatic brain injury)
Encephalitis
Guillain-Barré syndrome
Hemorrhagic stroke (intracerebral)
Ischemic stroke
Lumbar radiculopathy
Malignant spinal cord compression
Migraine
Peripheral neuropathy (acute)
Retropharyngeal abscess
Schizophrenia (acute exacerbation)
Seizure (breakthrough:known epilepsy)
Seizure (first-time)
Spinal cord injury
Status epilepticus
Subarachnoid hemorrhage
Tension headache
Transient ischemic attack
Traumatic brain injury (moderate-severe)
Vestibular neuritis
Viral meningitis
Gastrointestinal Presentations
Acute appendicitis
Acute cholecystitis
Acute diverticulitis
Acute pancreatitis
Anal fissure
Choledocholithiasis and cholangitis
Clostridioides difficile colitis
Gastritis
Gastroenteritis (viral and bacterial)
Gastroesophageal reflux disease
Incarcerated or strangulated hernia
Inflammatory bowel disease flare
Large bowel obstruction
Lower GI hemorrhage
Peptic ulcer disease
Perforated viscus
Small bowel obstruction
Upper GI hemorrhage
Genitourinary and Reproductive Presentations
Acute prostatitis
Acute urinary retention
Ectopic pregnancy
Epididymitis
Orchitis
Ovarian torsion
Paraphimosis
Pelvic inflammatory disease
Priapism
Pyelonephritis
Renal laceration
Ruptured ovarian cyst
Testicular torsion
Tubo-ovarian abscess
Urinary tract infection (uncomplicated)
Urolithiasis (renal colic)
Vaginal bleeding (non-pregnant)
Infectious Disease Presentations
Acute sinusitis
Acute tonsillitis
Acute upper respiratory infection
Animal bite
Bacterial meningitis
Cellulitis
Conjunctivitis (bacterial)
Dental abscess
Endocarditis
Febrile neutropenia
Fournier gangrene
Hand-foot-mouth disease
Hepatitis (acute)
Herpes zoster
HIV-related illness
Human bite
Impetigo
Infected diabetic foot ulcer
Infectious mononucleosis
Influenza
Necrotizing fasciitis
Osteomyelitis
Otitis externa
Parasitic infection
Periorbital cellulitis
Peritonsillar abscess
Scabies
Sepsis
Septic arthritis
Spontaneous bacterial peritonitis
Tick-borne illness (Lyme disease)
Tinea infection
Tuberculosis
Viral exanthem
Wound infection
Trauma Presentations
Achilles tendon rupture
ACL and mceniscus tear
Ankle fracture
Ankle sprain
Burn
Calcaneus fracture
Cervical spine fracture
Clavicle fracture
Dental avulsion
Distal radius fracture
Drowning
Elbow fracture and dislocation
Electrical injury
Facial bone fracture
Facial laceration
Femur fracture
Fingertip amputation
Forearm fracture (radius and ulna)
Frostbite
Hand:finger laceration
Heat exhaustion
Heat stroke
Hip fracture
Humeral shaft fracture
Knee dislocation
Knee sprain
Lightning injury
Mandible fracture
Metacarpal fracture
Metatarsal fracture
Muscle strain
Nasal fracture
Non-accidental trauma
Orbital fracture
Patella fracture
Phalanx fracture (finger)
Proximal humerus fracture
Pulmonary contusion
Rib fracture
Rotator cuff tear (acute traumatic)
Scalp laceration
Scaphoid fracture
Shoulder dislocation
Skull fracture
Splenic laceration
Sternal fracture
Supracondylar pediatric fracture
Tendon laceration (hand:wrist)
Thoracic and lumbar spine fracture
Tibia:fibula fracture
Tibial plateau fracture
Toe fracture
Traumatic epistaxis
Traumatic hyphema
Toxicologic Presentations
Acetaminophen toxicity
Alcohol intoxication
Alcohol withdrawal
Anticholinergic toxicity
Anticoagulant overdose
Benzodiazepine overdose
Benzodiazepine:sedative overdose
Beta-blocker and calcium channel blocker toxicity
Carbon monoxide poisoning
Caustic ingestion
Digoxin toxicity
Drug eruption
Foreign body ingestion
Opioid intoxication
Opioid overdose
Opioid withdrawal
Organophosphate
Salicylate toxicity
Serotonin syndrome
Stimulant intoxication (cocaine, methamphetamine)
Tricyclic antidepressant overdose
Psychiatric Presentations
Acute anxiety
Acute psychosis
Agitation:behavioral emergency
Bipolar disorder
Conversion disorder
Major depressive episode
Neuroleptic malignant syndrome
Suicidal ideation and attempt
Musculoskeletal and Rheumatologic Presentations
Acute low back pain (mechanical)
Bursitis
Cervical radiculopathy
Costochondritis
Gout (acute)
Lumbar radiculopathy
Pseudogout
Tendinitis
Dermatology Presentations
Acute eczema (Eczema acute flare)
Allergic contact dermatitis
Erythema multiforme
Henoch-Schönlein purpura
Pressure injury
Psoriasis (acute flare)
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Urticaria (acute)
Environmental and Exposure Presentations
Envenomation (snake, spider, insect)
High-altitude illness
Hypothermia
Hematologic and Oncologic Presentations
Acute chest syndrome
Coagulopathy
Hyperviscosity syndrome
Sickle cell crisis (vaso-occlusive)
Symptomatic anemia
Thrombocytopenia (severe)
Tumor lysis syndrome
Pediatric-Specific Presentations
Bronchiolitis
Croup
Emergency delivery
Febrile seizure
Kawasaki disease
Neonatal jaundice
Neonatal sepsis
Nursemaid's elbow
Pediatric fever 0 to 28 days
Pediatric fever 29 to 60 days
Pediatric fever 61 to 90 days
Pyloric stenosis
Slipped capital femoral epiphysis
Intussusception
Endocrine and Metabolic Presentations
Adrenal crisis
Diabetic ketoacidosis
Hypercalcemia
Hyperosmolar hyperglycemic state
Hypertensive emergency
Hypertensive urgency
Hypoglycemia
Myasthenia gravis crisis
Myxedema coma
Severe hyperkalemia
Severe hyponatremia
Thyroid storm
ENT and Maxillofacial Presentations
Acute laryngitis
Acute otitis media
Acute pharyngitis
Cerumen impaction
Epistaxis (anterior)
Nasal foreign body
Otitis externa
Tympanic membrane perforation
Ophthalmologic Presentations
Acute angle-closure glaucoma
Central retinal artery occlusion
Chemical eye injury
Corneal abrasion
Corneal ulcer
Globe rupture
Ocular foreign body
Orbital cellulitis
Retinal detachment
Obstetric Presentations
Hyperemesis gravidarum
Painful vaginal bleeding in pregnancy
Placenta previa
Placental abruption
Preeclampsia:eclampsia
Preterm labor
Threatened:inevitable:incomplete abortion
Systemic and Miscellaneous Presentations
Anaphylaxis
Angioedema
Cannabis-induced hyperemesis
Diffuse Axonal Injury (Severe)
POCUS
Procedures
Calculators
Resuscitation
ECG Guide
Back
Clinical Assessment Checklist
Browse categories and answer follow-up questions to refine your symptom profile.
Approach to the Critical Patient
Immediate priorities
Airway and ventilation
▶
Rapid sequence intubation for GCS <= 8
▶
Target SpO2 > 90% at all times
Avoid hypoxia as independent predictor of poor outcome
C-spine immobilization until cleared
▶
Inline stabilization during intubation
CT C-spine mandatory in all severe TBI
Post-intubation ventilator targets
▶
PaCO2 35 to 38 mmHg (normocapnia)
Avoid hypocapnia except for impending herniation rescue
Hemodynamic stabilization
▶
SBP target > 100 mmHg (age >= 50: > 110 mmHg)
▶
Hypotension doubles mortality in severe TBI
Crystalloid resuscitation first line
CPP target 60 to 70 mmHg when ICP monitored
▶
MAP augmentation if CPP inadequate
Vasopressors for refractory hypotension
Avoid hypertonic glucose solutions
▶
Isotonic or slightly hypertonic fluids preferred
Target euvolemia
Herniation recognition and response
▶
Cushing triad: hypertension, bradycardia, irregular respirations
▶
Immediate osmotherapy
Emergent neurosurgical notification
Acute pupillary dilation (unilateral or bilateral)
▶
Hyperventilate to PaCO2 30 to 35 mmHg as bridge
Mannitol 1 g/kg IV bolus
Monitoring and targets
Monitoring bundle
▶
Continuous pulse oximetry
▶
SpO2 > 90% mandatory floor
Arterial line for continuous blood pressure monitoring
ICP monitoring for GCS <= 8
▶
Parenchymal probe or external ventricular drain (EVD)
ICP target < 22 mmHg (BTF Grade B recommendation)
End-tidal CO2 monitoring
▶
Correlate with PaCO2 via ABG
Avoid inadvertent hyperventilation
Continuous EEG monitoring
▶
Subclinical seizures in up to 25% of severe TBI patients
Spreading depolarizations detection
Temperature management
▶
Normothermia target 36 to 37 degrees C
▶
Hyperthermia increases metabolic demand and ICP
Antipyretics and cooling blanket as needed
Therapeutic hypothermia not recommended for routine use
▶
Adverse effects outweigh benefit in most trials
CRASH-2 and cooling trial evidence
Immediate consults
Consultation triggers
▶
Neurosurgery mandatory for all severe TBI
▶
ICP monitor placement
EVD consideration for hydrocephalus or high ICP
Neurology or neurointensive care
▶
EEG interpretation
Seizure management
Trauma surgery
▶
Polytrauma management
Hemorrhage control coordination
Transfer to Level I trauma center if not already present
▶
Neurosurgical capability required
BTF and ACS best practice recommendation
History
Mechanism and event
Mechanism characteristics
▶
High-speed motor vehicle collision
▶
Most common cause of DAI
Ejection from vehicle significantly increases severity
Motorcycle or bicycle crash without helmet
▶
Unrestrained head acceleration
Higher Grade 3 DAI risk
High fall
▶
Height of fall
Surface type at landing
Blast injury
▶
Military or industrial exposure
Primary blast wave mechanism
Assault
▶
Weapon used
Non-accidental trauma consideration
Loss of consciousness
▶
Immediate and sustained from moment of impact
▶
Distinguishes DAI from mass lesion where lucid interval may occur
Duration of coma > 24 hours with brainstem signs defines severe category
Witness account of impact
▶
Vehicle speed estimation
Airbag deployment or helmet use
Duration of unconsciousness at scene
Pre-injury context
Medications and substances
▶
Anticoagulant use
▶
Increases hemorrhagic component of DAI
Warfarin, DOAC, antiplatelet agents
Antiplatelet agents
▶
Aspirin, clopidogrel
Reversal strategy consideration
Alcohol intoxication at time of injury
▶
Confounds GCS assessment
Blood alcohol level needed for accurate neurological baseline
Past medical history
▶
Prior TBI or concussions
▶
Cumulative axonal vulnerability
Baseline cognitive reserve impact
Pre-existing neurological conditions
▶
Dementia affects outcome prognostication
Epilepsy influences seizure management
Chronic alcohol use
▶
Brain atrophy increases shearing vulnerability
Subdural hygroma risk
Advance care planning
▶
Advance directives or healthcare proxy
▶
Critical for goals-of-care discussions in prolonged coma
Early family notification required
Premorbid functional status
▶
Affects rehabilitation candidacy
Influences outcome expectations
Associated injury clues
Polytrauma screen
▶
C-spine pain or tenderness
▶
High-energy mechanism implies C-spine until cleared
Concurrent cord injury alters management
Chest or abdominal trauma
▶
Hemothorax or pneumothorax
Solid organ injury with hemorrhage
Long bone fractures
▶
Fat embolism syndrome risk (delayed onset 24 to 72 hours)
Petechial rash and hypoxia
Scalp laceration or skull deformity
▶
Open head injury
Depressed skull fracture
Physical Exam
Neurological assessment
GCS components (document separately)
▶
Eye opening
▶
4 spontaneous, 3 to voice, 2 to pain, 1 none
Periorbital swelling may falsely lower eye score
Verbal response
▶
Intubation assigns V score of 1T (scored as 1)
Baseline language function from family history
Motor response
▶
Motor score 1 to 2 (posturing) indicates severe injury
Asymmetry suggests concurrent focal lesion
Pupillary assessment
▶
Bilateral fixed dilated pupils
▶
Suggests Grade 3 brainstem DAI
Or bilateral uncal herniation
Unilateral dilation
▶
Raises concern for concurrent hematoma and herniation
Surgical emergency differentiation
Pupillometry quantitative assessment
▶
Neurological Pupil index (NPi) aids ICP detection
Serial trend more informative than single measurement
Posturing patterns
▶
Decerebrate posturing (extension)
▶
Brainstem level injury
Worst prognostic posturing pattern
Decorticate posturing (flexion)
▶
Subcortical or thalamic level
Better prognosis than decerebrate
Brainstem reflexes
Reflex assessment sequence
▶
Corneal reflex
▶
Absence suggests pontine level dysfunction
Bilateral loss is concerning for deep injury
Oculocephalic reflex (doll's eyes)
▶
Only if C-spine cleared
Absence indicates brainstem dysfunction
Oculovestibular reflex (calorics)
▶
Cold water caloric test
Most sensitive brainstem reflex test
Gag and cough reflex
▶
Medullary function assessment
Relevant for airway protection prognosis
Systemic exam
Vital signs pattern
▶
Cushing response: hypertension with bradycardia
▶
Critically elevated ICP marker
Irregular respirations as third component
Paroxysmal sympathetic hyperactivity (PSH)
▶
Episodic tachycardia, hypertension, diaphoresis
Posturing and hyperthermia episodes
Trauma survey
▶
HEENT and scalp
▶
Lacerations and bony deformity
Battle sign or raccoon eyes (basilar skull fracture)
Chest and abdomen
▶
Tension pneumothorax exclusion
Hemothorax or rib fractures
Pelvis and extremities
▶
Long bone fracture identification
Vascular injury screen
Differential Diagnosis
Life threats
Competing diagnoses requiring immediate surgical consideration
▶
Epidural hematoma
▶
ICD-10 S06.4
Lucid interval followed by deterioration
Biconvex density on CT
Acute subdural hematoma
▶
ICD-10 S06.5
Crescent density along brain surface
Often with underlying cortical injury
Intracerebral hemorrhage or contusion
▶
ICD-10 S06.3
Frontal and temporal poles most common
Mass effect and midline shift
Diffuse cerebral edema
▶
Loss of gray-white differentiation on CT
Elevated ICP from swelling rather than hematoma
DAI mimics
Diagnoses that can cause coma after trauma without structural lesion
▶
Hypoxic-ischemic brain injury
▶
Post-cardiac arrest or prolonged hypotension during trauma
Diffuse cortical and basal ganglia restriction on DWI
Toxic or metabolic encephalopathy
▶
Drug intoxication, hypoglycemia, severe hyponatremia
Must be excluded before attributing coma to DAI
Non-convulsive status epilepticus
▶
ICD-10 G41.9
Requires continuous EEG for diagnosis
Can mimic persistent vegetative state
Fat embolism syndrome
▶
Delayed onset 24 to 72 hours after long bone fracture
Petechial rash and hypoxia with altered consciousness
Cerebral venous sinus thrombosis
▶
Atypical mechanism or progressive course
CT venography or MR venography for diagnosis
DAI grading by distribution
Anatomical classification (Adams)
▶
Grade 1 (lobar white matter, gray-white junction)
▶
ICD-10 S06.2 diffuse traumatic brain injury
Best prognosis; mean time to follow commands approximately 9 days
Grade 2 (corpus callosum involvement plus Grade 1 lesions)
▶
Intermediate prognosis
OR 2.9 per grade increase for unfavorable outcome
Grade 3 (brainstem involvement plus Grades 1 to 2 lesions)
▶
Worst prognosis; median GOSE 4 at 1 year
8-fold increased risk of poor functional outcome
Laboratory Tests
Trauma and resuscitation labs
Immediate stat panel
▶
Complete blood count
▶
Hemoglobin for transfusion threshold
Platelet count; < 100 x10^9/l requires correction
Coagulation panel
▶
PT/INR > 1.5 requires urgent correction
Fibrinogen < 2 g/l requires cryoprecipitate
Comprehensive metabolic panel
▶
Sodium monitoring for SIADH and diabetes insipidus
Glucose target 5.6 to 10 mmol/l (avoid hypoglycemia)
Type and screen
▶
Blood product preparation for hemorrhagic component
Crossmatch if active hemorrhage
Perfusion and metabolic monitoring
Lactate
▶
>= 2 mmol/l indicates hypoperfusion
▶
Serial monitoring every 2 to 4 hours if elevated
Clearance target within 6 hours
Arterial blood gas
▶
PaCO2 mmHg for ventilator titration
▶
Target 35 to 38 mmHg
Avoid PaCO2 < 30 mmHg except brief herniation rescue
PaO2 > 80 mmHg target
▶
Hyperoxia may worsen secondary injury; avoid FiO2 1.0 unnecessarily
Pulse oximetry confirmed with intermittent ABG
Blood alcohol level
▶
Confounds GCS assessment
▶
Significant BAC level reduces apparent neurological score
Repeat neuro exam as alcohol clears
Biomarkers
GFAP (glial fibrillary acidic protein)
▶
FDA-cleared for ruling out intracranial hemorrhage
▶
Peaks approximately 20 hours after injury
Elevated levels correlate with injury severity and mortality
Prognostic value for functional recovery (TRACK-TBI cohort)
▶
Day-of-injury plasma level predicts 6-month outcome
Higher levels predict worse GOSE scores
UCH-L1 (ubiquitin C-terminal hydrolase L1)
▶
Neuronal injury marker
▶
Peaks approximately 8 hours after injury
FDA-cleared in combination with GFAP
Elevated in DAI correlating with lesion burden
▶
Use as adjunct not standalone decision tool
ACEP Level B recommendation for biomarker use in TBI evaluation
Neurofilament light chain (NfL)
▶
Emerging prognostic biomarker
▶
Strongest association with 6-month poor outcome
Not yet FDA-cleared for clinical decision use
Ongoing meta-analysis data (Mondello et al. 2025)
Endocrine and electrolyte monitoring
Serum sodium serial monitoring
▶
SIADH (hyponatremia)
▶
Na < 135 mmol/l in up to 30% of severe TBI
Fluid restriction and hypertonic saline management
Diabetes insipidus (hypernatremia)
▶
Na > 145 mmol/l with dilute urine
Pituitary stalk injury in severe DAI
Pituitary function screen
▶
Cortisol for adrenal insufficiency
▶
Random cortisol < 276 nmol/l suggests insufficiency
Hydrocortisone supplementation if confirmed
Thyroid function
▶
Sick euthyroid in acute phase
True secondary hypothyroidism requires treatment
Diagnostic Tests
Scoring Systems
DAI grading and TBI severity tools
▶
Adams DAI Classification (Grades 1 to 3)
▶
Grade 1: lobar white matter only
Grade 2: corpus callosum involvement
Grade 3: brainstem involvement (worst prognosis)
GCS score at admission
▶
Severe TBI defined as GCS <= 8
Motor subscale most prognostically powerful component
Confounders: intubation, sedation, alcohol, hypotension
IMPACT Prognostic Calculator
▶
Validated model incorporating age, GCS motor, pupillary reactivity
CT classification and biomarkers incorporated
Predicts 6-month GOSE and mortality
Rotterdam CT Score
▶
CT-based prognostic tool for TBI
Incorporates basal cistern status, midline shift, epidural hematoma
Higher score predicts worse outcome
Marshall CT Classification
▶
Diffuse injury I to IV categories
Mass lesion evacuated or not evacuated categories
Widely used in clinical research for outcome prediction
Functional outcome scales
▶
Glasgow Outcome Scale Extended (GOSE)
▶
1 (death) to 8 (upper good recovery)
GOSE >= 6 considered favorable outcome
51% of DAI patients achieve favorable outcome (van Eijck et al.)
Disability Rating Scale (DRS)
▶
0 (no disability) to 29 (extreme vegetative state)
Useful for tracking rehabilitation progress
MRI
MRI brain sequences for DAI (gold standard when patient stable)
▶
SWI or T2-GRE sequence
▶
Most sensitive for hemorrhagic microbleeds
Hemosiderin deposits at gray-white junction, corpus callosum, brainstem
Detects lesions invisible on CT (sensitivity superior to CT)
FLAIR sequence
▶
Non-hemorrhagic white matter lesions
Hyperintense signal in injured axonal tracts
Sensitive for corpus callosum and deep white matter injury
DWI/ADC sequence
▶
Restricted diffusion in acute axonal injury
ADC maps characterize cytotoxic vs vasogenic edema
Early DWI lesions predict poor outcome
T1-weighted sequence
▶
Structural anatomy
Chronic changes and atrophy on follow-up
Diffusion Tensor Imaging (DTI)
▶
Quantifies white matter tract integrity
Fractional anisotropy reduction in injured tracts
Currently research tool; emerging clinical use
MRI timing and indications
▶
Acute phase: when hemodynamically stable and able to safely transport
▶
Provides definitive DAI grading not possible on CT
ACR Appropriateness Criteria: Usually Appropriate for coma evaluation
Subacute phase (7 to 14 days)
▶
Full lesion burden visible as edema resolves
Prognostication and rehabilitation planning
Follow-up MRI
▶
Assess for hydrocephalus, encephalomalacia
DTI for white matter tract recovery assessment
CT
CT head non-contrast (immediate first-line imaging)
▶
Common CT findings in DAI
▶
Punctate hemorrhages at gray-white junction
Corpus callosum hemorrhage
Brainstem petechial hemorrhages
Intraventricular hemorrhage
Key clinical pearl: CT often normal or near-normal in pure DAI
▶
Comatose patient with normal CT after high-energy mechanism raises strong DAI suspicion
Sensitivity of CT for DAI approximately 20 to 50%; MRI detects far more lesions
Traumatic midline subarachnoid hemorrhage on CT
▶
Sensitivity 60.8% and specificity 81.7% as surrogate marker for severe DAI
Mata-Mbemba et al. 2018 evidence
CT C-spine
▶
Mandatory in all severe TBI
▶
Cannot clinically clear C-spine in comatose patient
High sensitivity multi-detector CT preferred
CT head and C-spine typically obtained simultaneously
▶
Minimizes transport and time to diagnosis
Polytrauma protocol CT if hemodynamically stable
CT angiography head and neck
▶
Indications for vascular injury screening
▶
High-energy mechanism with neck involvement
Vertebral or carotid territory signs
Traumatic dissection or pseudoaneurysm exclusion
▶
Significant management implication
Anticoagulation or stenting decision
Serial CT head
▶
Repeat within 6 to 24 hours if initial CT has any hemorrhagic lesion
▶
Expansion of hematoma risk in first 24 hours
Sooner if neurological deterioration
ICP trend correlation
▶
Radiographic worsening may precede clinical change
Ultrasound
Optic nerve sheath diameter (ONSD)
▶
Bedside ultrasound technique
▶
ONSD > 5 mm suggests elevated ICP (> 20 mmHg)
3 mm posterior to globe measurement standard
Utility in resource-limited or pre-imaging settings
▶
Sensitivity approximately 74% to 90% for elevated ICP
Use as adjunct to clinical exam not replacement for ICP monitoring
Serial ONSD for ICP trend monitoring
▶
Operator-dependent limitation
Correlate with clinical findings and formal ICP values
FAST and extended FAST (eFAST)
▶
Polytrauma evaluation
▶
Pericardial effusion or tamponade
Pneumothorax (eFAST)
Hemoperitoneum assessment
Hemodynamic shock source identification
▶
Rules out competing hemorrhagic sources
Integrates with trauma bay primary survey
Transcranial Doppler (TCD)
▶
Cerebral blood flow velocity assessment
▶
Vasospasm detection (delayed > 3 days)
Pulsatility index correlates with ICP
Brain death evaluation adjunct
▶
Reverberant or systolic spike pattern
Requires confirmatory formal testing
Disposition
ICU admission
All severe DAI patients require ICU admission
▶
ICP monitoring mandatory for GCS <= 8
▶
Parenchymal probe or EVD placement
BTF Level B recommendation
Neurosurgical team involvement
▶
ICP monitor insertion
Surgical management if secondary hematoma develops
Neuro-ICU preferred over general ICU when available
▶
Specialized nursing and monitoring protocols
Dedicated neurointensive care team
Transfer criteria
▶
Transfer to Level I trauma center if not currently present
▶
Neurosurgical capability mandatory
Neurointensive care capability preferred
Stabilize before transfer
▶
Airway secured and ventilation adequate
Hemodynamic stability or vasopressors running
ICP managed during transport
ICU course planning
Duration of ICU stay
▶
Grade 1 DAI: median approximately 6 days
▶
Time to follow commands approximately 9 days
Transition to step-down when ICP controlled
Grade 2 to 3 DAI: prolonged ICU course
▶
Median time to commands approximately 19 days for Grade 3
Tracheostomy and PEG planning often required
Ongoing ICP monitoring duration
▶
Continue until ICP stable < 22 mmHg without intervention for 24 to 48 hours
Remove monitor after stable period
Rehabilitation transition
▶
Acute inpatient rehabilitation when medically stable
▶
Able to participate minimally (even inconsistently)
Tracheostomy weaning and PEG feeding compatible with rehab
Avoid premature withdrawal of life-sustaining treatment
▶
Recovery can occur weeks to months after injury
Particularly important in younger patients
Prognosis communication
Goals-of-care discussion timing
▶
Early family meeting within 24 to 48 hours
▶
Prognostic humility essential
Avoid definitive prognosis in first 72 hours
51% of DAI patients achieve favorable long-term outcome (GOSE 6 to 8)
▶
Van Eijck et al. Journal of Neurotrauma 2018
Even Grade 3 patients can achieve meaningful recovery
Functional improvement most pronounced in first 3 months
▶
Gains continue for 1 to 2 years
Family counseling for prolonged recovery trajectory
Treatment
Initial ED stabilization
Airway management
▶
Rapid sequence intubation
▶
Ketamine 1.5 to 2 mg/kg IV (hemodynamically preferred)
Etomidate 0.3 mg/kg IV alternative
Succinylcholine 1.5 mg/kg IV for paralysis unless contraindicated
Post-intubation sedation
▶
Propofol 5 to 50 mcg/kg/min IV infusion
▶
Titrate to ICP control and RASS score
Propofol infusion syndrome risk with prolonged high dose
Midazolam 0.02 to 0.1 mg/kg/h IV infusion alternative
▶
Accumulation risk with prolonged use
Renal and hepatic monitoring required
Analgesia
▶
Fentanyl 25 to 50 mcg IV PRN bolus for procedures
▶
Continuous infusion 25 to 100 mcg/h if needed
Minimize opioids when possible (ICP effects)
Coagulopathy correction
▶
Warfarin reversal
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4-factor PCC (Kcentra) 25 to 50 units/kg IV
Vitamin K 10 mg IV concurrent
DOAC reversal
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Dabigatran: idarucizumab 5 g IV
Factor Xa inhibitors: andexanet alfa or 4F-PCC
Platelet transfusion if count < 100 x10^9/l with hemorrhagic lesion
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Target platelets > 100 x10^9/l for active bleeding
1 apheresis unit typical initial dose
Cryoprecipitate for fibrinogen < 2 g/l
▶
10-unit pool typically raises fibrinogen 1 g/l
Recheck level after replacement
ICP management (tiered SIBICC approach)
Tier 0 (basic care for all severe TBI)
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Head of bed 30 degrees, head midline
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Promotes venous drainage
Avoid hip flexion > 90 degrees
Normothermia target 36 to 37 degrees C
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Acetaminophen 650 mg IV or PO every 6 hours PRN
Cooling blanket for refractory hyperthermia
Euvolemia maintenance
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Isotonic crystalloid to maintain MAP
Avoid hypotonic fluids (worsen cerebral edema)
Seizure prophylaxis 7 days
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Levetiracetam 500 to 1000 mg IV every 12 hours
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Renal dose adjustment required
Preferred over phenytoin (fewer drug interactions)
Phenytoin 100 mg IV every 8 hours alternative
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Therapeutic drug monitoring required
QT monitoring needed
Tier 1 (ICP 22 to 30 mmHg)
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Increase sedation and analgesia
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Propofol dose increase to RASS -3 to -4
Fentanyl infusion for pain-mediated ICP spikes
Osmotherapy
▶
Mannitol 0.25 to 1.0 g/kg IV bolus
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Serum osmolality limit 320 mOsm/kg
Avoid if serum osmolality already > 310 mOsm/kg
Hypertonic saline 3% NaCl 250 mL IV bolus alternative
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Target serum sodium 145 to 155 mmol/l
Central line preferred for concentrations > 3%
CSF drainage via EVD if in place
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5 to 10 mL aliquots to reduce ICP
Monitor for infection with prolonged use
CPP target 60 to 70 mmHg
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Norepinephrine for MAP augmentation if needed
Start at 0.05 mcg/kg/min, titrate to CPP target
Tier 2 (ICP > 30 mmHg refractory to Tier 1)
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Mild hyperventilation
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PaCO2 32 to 35 mmHg as temporary measure
Not sustained > 24 hours without cerebral perfusion monitoring
Neuromuscular blockade
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Cisatracurium 0.1 to 0.2 mg/kg/h infusion
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Trial dose 0.1 mg/kg IV first
EEG monitoring while paralyzed
Rocuronium alternative for shorter duration trials
MAP augmentation
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Norepinephrine titrated to CPP 60 to 70 mmHg
Phenylephrine for tachycardia with CPP deficit
Tier 3 (refractory elevated ICP > 30 mmHg)
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Barbiturate coma
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Pentobarbital 5 to 10 mg/kg IV load over 30 minutes
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Maintenance 1 to 4 mg/kg/h infusion
Titrate to burst suppression on EEG
Hypotension is major adverse effect requiring vasopressors
Decompressive craniectomy
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Bifrontal or unilateral depending on injury pattern
Rescue option for refractory ICP
DECRA and RESCUEicp trial evidence informs decision
Mild hypothermia 35 to 36 degrees C
▶
Last resort after failure of other tiers
Rewarming protocol critical to avoid rebound ICP
Medications to avoid
Corticosteroids are contraindicated in severe TBI
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CRASH trial demonstrated increased mortality
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Methylprednisolone 2 g IV bolus increased 2-week mortality
Relative risk 1.18 (95% CI 1.09 to 1.27)
Class I recommendation against corticosteroid use
Routine hypothermia not recommended
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Adverse effects outweigh benefit in most trials
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Infection risk and hemodynamic instability
Eurotherm3235 trial showed harm
Paroxysmal sympathetic hyperactivity treatment
PSH recognition and management
▶
Clinical criteria
▶
Episodic tachycardia HR > 120 beats/min
Hypertension SBP > 160 mmHg
Diaphoresis, hyperthermia, tachypnea, posturing
Pharmacological management
▶
Propranolol 20 to 60 mg PO every 6 hours
▶
Beta-1 and beta-2 blockade reduces sympathetic surge
Titrate to heart rate reduction
Bromocriptine 2.5 to 5 mg PO every 8 hours
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Dopaminergic mechanism
First-line for PSH in many centers
Clonidine 0.1 mg PO every 8 hours
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Central alpha-2 agonist reduces sympathetic outflow
Sedation risk monitoring required
Gabapentin 300 mg PO TID titrated to 1200 to 3600 mg/day
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Reduces paroxysmal episodes
Renal dose adjustment required
Opioid PRN for acute severe episodes
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Morphine 2 to 4 mg IV PRN
Covers sympathetic storms during procedures
VTE prophylaxis
Pharmacologic VTE prophylaxis
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Initiate when safe typically 24 to 72 hours post-injury
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Guided by repeat imaging stability (no hematoma expansion)
Neurosurgery approval required
Enoxaparin 40 mg subcutaneous daily
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Renal dose adjustment for CrCl < 30 mL/min
Anti-Xa monitoring in obesity and renal insufficiency
Unfractionated heparin 5000 units subcutaneous every 8 hours alternative
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If enoxaparin contraindicated
More easily reversible with protamine
Mechanical VTE prophylaxis
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Sequential compression devices from admission
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Applied to all extremities without injury
Continue until ambulatory or pharmacologic prophylaxis started
Nutritional support
Early enteral nutrition within 24 to 72 hours
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BTF guideline recommendation for mortality reduction
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Caloric target 140% of resting metabolic expenditure in non-paralyzed patients
Caloric target 100% in paralyzed patients
Nasogastric tube placement if not intubated with NG
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Post-pyloric tube if gastroparesis
PEG tube for prolonged requirement
Glucose monitoring and control
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Target 5.6 to 10 mmol/l
Hypoglycemia particularly harmful to injured brain
Insulin infusion protocol for hyperglycemia
Special Populations
Pregnancy
Physiologic considerations
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Hemodynamic changes in pregnancy
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Increased blood volume reduces apparent blood loss
Hypotension occurs later but is more dangerous for fetus
Uterine displacement
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Left lateral tilt to relieve aortocaval compression
SBP target > 90 mmHg critical for placental perfusion
Radiation exposure
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CT head acceptable given life-threatening indication
MRI preferred when clinically equivalent and available
Abdominal shielding for CT head and neck
Medication considerations
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Mannitol
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Risk of fetal dehydration and hypernatremia
Use only for acute herniation threat
Hypertonic saline may be preferred alternative
Levetiracetam
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Limited teratogenicity data; use if seizure prophylaxis required
Weigh benefit against risk; life-threatening injury justifies use
Sedation agents
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Propofol: avoid prolonged high-dose in pregnancy
Fentanyl: neonatal respiratory depression risk with prolonged use
Fetal monitoring
▶
Viable gestation (>= 24 weeks): continuous fetal monitoring
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Obstetrics consultation immediately
Emergency cesarean section readiness if fetal distress
Pre-viable gestation: maternal stabilization is priority
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Fetal outcome depends on maternal outcome
Geriatric
Age-related vulnerability
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Brain atrophy increases bridging vein tension
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Higher subdural hematoma risk with smaller mechanism
Larger subdural tolerated before symptoms due to space
Reduced cerebrovascular autoregulation
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Narrower CPP target range
Hypotension poorly tolerated
Higher baseline white matter disease
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Confounds MRI DAI interpretation
Pre-existing cognitive impairment affects outcome baseline
Medication and coagulation considerations
▶
High anticoagulant use in elderly population
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Immediate reversal of all anticoagulants required
DOAC prevalence increasing; reversal agents now available
Antiplatelet agent use
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Clopidogrel or aspirin
Platelet transfusion if intracranial hemorrhage present
Polypharmacy sedation risk
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Benzodiazeines and opioids titrated carefully
Delirium risk in ICU extremely high
Prognosis in elderly
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Age is independent predictor of poor outcome in IMPACT model
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Older age increases odds of unfavorable outcome at 6 months
Age alone should not drive withdrawal decisions
Early goals-of-care discussion
▶
Advance directives more commonly exist in elderly
Functional baseline is key to prognosis communication
Pediatrics
Mechanism-specific considerations
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Non-accidental trauma (NAT) must be excluded
▶
Shaken baby syndrome causes DAI in infants
Pattern of injuries inconsistent with stated mechanism
Child protective services notification mandatory when suspected
Age-specific mechanisms
▶
Motor vehicle collision most common in adolescents
Sports injury in school-age children
High falls in toddlers
Physiologic differences
▶
ICP management targets age-adjusted
▶
Neonates and infants: ICP < 15 mmHg target
Children: ICP < 20 mmHg target (similar to adult for age >= 6)
Blood pressure targets
▶
SBP target at least 5th percentile for age
Hypotension thresholds lower than adults
Brain plasticity
▶
Better long-term recovery potential than adults for equivalent injury
Ferrazzano et al. JAMA Network Open 2024 pediatric outcome data
Weight-based dosing
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Mannitol 0.25 to 1.0 g/kg IV per dose (same per-kg dosing as adult)
▶
Osmolality limit 320 mOsm/kg same threshold
Levetiracetam 20 to 30 mg/kg IV load then 10 to 20 mg/kg IV every 12 hours
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Renal adjustment applies
Hypertonic saline 3% NaCl 5 mL/kg IV over 30 minutes for acute ICP crisis
▶
Repeat as needed with sodium monitoring
Target sodium 145 to 155 mmol/l
Rehabilitation considerations
▶
Multidisciplinary pediatric rehabilitation team
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School reintegration planning early
Neuropsychological testing for cognitive recovery tracking
MRI-based outcome prediction validated in pediatrics
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Ferrazzano 2024: MRI + clinical variables predict 6-month outcome
Corpus callosum and brainstem lesions on MRI most predictive
Background
Epidemiology
Incidence and distribution
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DAI found in up to 50% of severe TBI cases
▶
Prevalence increases with injury severity
Grade 3 brainstem DAI found in approximately 16% of severe TBI
Peak incidence in young males 15 to 35 years
▶
Motor vehicle collision most common mechanism
Male-to-female ratio approximately 3:1
Second peak in elderly patients
▶
Falls predominant mechanism
Higher concurrent subdural hematoma frequency
Mortality and morbidity
▶
In-hospital mortality for severe TBI ranges 25 to 50%
▶
Grade 3 DAI carries highest mortality
Brainstem involvement is strongest negative prognostic factor
Long-term functional outcomes
▶
51% achieve favorable GOSE 6 to 8 at long-term follow-up
Van Eijck et al. Journal of Neurotrauma 2018 meta-analysis
Persistent disability common in survivors
▶
Cognitive, behavioral, emotional sequelae
Post-traumatic epilepsy in approximately 10 to 17%
Pathophysiology
Primary injury mechanisms
▶
Rapid rotational acceleration-deceleration forces
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Angular forces exceed tensile strength of axons
Most vulnerable at regions of different tissue density interfaces
Axonal stretching and disruption
▶
Initial axolemmal permeability change (mechanoporation)
Calcium influx triggers mitochondrial dysfunction
Progressive axonal swelling and disconnection over hours
Distribution by tissue density differences
▶
Gray-white junction (lobar, Grade 1)
Corpus callosum (Grade 2)
Brainstem and dorsolateral midbrain (Grade 3)
Secondary injury mechanisms
▶
Excitotoxicity
▶
Glutamate release from damaged neurons
NMDA receptor activation and calcium overload
Mitochondrial dysfunction
▶
Oxidative stress and energy failure
Initiates apoptotic cascades
Neuroinflammation
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Microglial activation within hours
Prolonged inflammatory response contributes to white matter loss
Axonal transport failure
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Impaired axoplasmic flow
Axonal retraction balls form (beta-APP accumulation)
DAI vs hemorrhagic contusion distinction
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Pure DAI: CT often normal; MRI reveals white matter lesions
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No surgical target (unlike hematomas)
Management entirely medical
Hemorrhagic DAI: microbleeds visible on SWI
▶
CT demonstrates only larger hemorrhagic components
CT hemorrhagic DAI not associated with worse CT-based outcome
Henninger et al. J Trauma Acute Care Surg 2018
Therapeutic Considerations
ICP management evidence base
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BTF 4th edition guidelines (2016)
▶
ICP threshold 22 mmHg for treatment (Level B)
CPP target 60 to 70 mmHg (Level B)
Decompressive craniectomy as rescue for refractory ICP
SIBICC consensus algorithm (Hawryluk et al. 2019)
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Tiered treatment approach for ICP management
Escalating interventions based on ICP response
No proven neuroprotective agents for DAI
▶
Multiple agents failed in clinical trials (progesterone, magnesium, ciclosporin)
Prevention of secondary injury remains therapeutic focus
Biomarker-guided management
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GFAP and UCH-L1 for injury characterization
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FDA cleared for ruling out intracranial hemorrhage in TBI
TRACK-TBI study: day-of-injury levels predict 6-month GOSE
NfL as emerging prognostic biomarker
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Living meta-analysis (Mondello et al. 2025) shows strongest outcome correlation
Not yet in clinical guideline recommendations
Rehabilitation and recovery
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Early rehabilitation initiation improves outcomes
▶
Passive range of motion and positioning from ICU day 1
Sensory stimulation program in disorders of consciousness
Disorders of consciousness management
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Minimally conscious state vs vegetative state distinction
Amantadine 100 to 200 mg PO BID for MCS acceleration
Zolpidem trial (paradoxical activation) reported in anecdotal series
Long-term complications monitoring
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Post-traumatic epilepsy risk persists beyond 7-day prophylaxis window
Neuroendocrine dysfunction in up to 30%
Chronic traumatic encephalopathy (CTE) long-term concern
Patient Discharge Instructions
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For patients and families of severe DAI survivors being discharged to rehabilitation
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Understanding the diagnosis
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Diffuse axonal injury is damage to the nerve fibers of the brain caused by the injury
Recovery is a slow process that continues for months to years
Most improvement occurs in the first 3 to 6 months but gains continue for 1 to 2 years
What to expect during recovery
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Periods of confusion, agitation, or behavioral changes are common
Fatigue is expected and rest is important
Physical, occupational, and speech therapy are the primary treatments
Rehabilitation instructions
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Attend all scheduled rehabilitation sessions
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Physical therapy for mobility and strength
Occupational therapy for daily living skills
Speech language pathology for communication and swallowing
Home environment safety
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Remove fall hazards from home
Supervision required for all activities until cleared by rehabilitation team
Do not drive until formally evaluated and cleared by physician
Medications
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Take all prescribed medications exactly as directed
Do not stop seizure medications without physician approval
Avoid alcohol completely during recovery
Return to emergency department immediately for
▶
New seizure or prolonged convulsion
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Any shaking episode lasting more than 5 minutes
First seizure after injury
Sudden worsening of consciousness or responsiveness
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Difficulty awakening the patient
Significant new confusion
Severe new headache or vomiting
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Headache much worse than baseline
Repeated vomiting without known cause
New weakness or numbness
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One side of body weaker than baseline
Facial droop or speech change
Signs of infection
▶
Fever > 38.5 degrees C
Redness or drainage from surgical wound if applicable
Behavioral changes suggesting hydrocephalus
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Progressive sleepiness over days
Worsening cognition after initial improvement
Follow-up appointments
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Neurosurgery follow-up within 2 weeks of discharge
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Review of MRI findings and imaging if not yet completed
ICP monitor wound check if applicable
Neurology for seizure monitoring
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EEG if clinically indicated
Medication adjustment as needed
Neuropsychology assessment at 3 to 6 months
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Cognitive and behavioral testing
Return-to-work or school planning
Neuroendocrine screening at 3 to 6 months
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Pituitary hormone panel
Endocrinology referral if abnormal
References
Guidelines and key sources
Primary guidelines
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Brain Trauma Foundation 4th Edition Guidelines 2016
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ICP and CPP management thresholds
Decompressive craniectomy evidence
Seattle International Severe TBI Consensus Conference (SIBICC) 2019
▶
Hawryluk et al. Intensive Care Medicine 2019
Tiered ICP management algorithm
American College of Surgeons Best Practices TBI 2024
▶
Manley et al. comprehensive TBI management
Coagulopathy correction protocols
ACR Appropriateness Criteria Head Trauma 2021
▶
Shih et al. Journal of American College of Radiology
MRI and CT indications for severe TBI
Landmark studies
Prognostic studies
▶
Van Eijck et al. Journal of Neurotrauma 2018
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51% of DAI patients achieve favorable long-term functional outcome
GOSE 6 to 8 achievable even after Grade 3 DAI
Ferrazzano et al. JAMA Network Open 2024
▶
MRI and clinical variables predict pediatric severe TBI outcomes
Corpus callosum and brainstem lesions most predictive
Skandsen et al. Journal of Neurosurgery 2010
▶
Prevalence and impact of DAI in moderate and severe TBI cohort
MRI-detected DAI vs CT findings correlation
Biomarker studies
▶
Korley et al. Lancet Neurology 2022
▶
TRACK-TBI cohort; GFAP and UCH-L1 day-of-injury values predict 6-month recovery
Mondello et al. Journal of Neurotrauma 2025
▶
Living meta-analysis of blood-based biomarkers in TBI
NfL has strongest association with poor outcome
Papa et al. JAMA Neurology 2016
▶
Time course and diagnostic accuracy of GFAP and UCH-L1
Treatment studies
▶
CRASH trial (corticosteroids)
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Roberts et al. Lancet 2004
Methylprednisolone increased 2-week mortality (RR 1.18)
Mata-Mbemba et al. Journal of Neurosurgery 2018
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Traumatic midline SAH as CT surrogate for severe DAI
Sensitivity 60.8% specificity 81.7%
El-Abtah et al. World Neurosurgery 2023
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DAI pattern predicts timing of in-hospital neurological recovery
Coding references
ICD-10 coding
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S06.2 Diffuse traumatic brain injury
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S06.2X0A: without loss of consciousness, initial encounter
S06.2X9A: with loss of consciousness of unspecified duration
S06.4 Epidural hemorrhage (differential)
S06.5 Traumatic subdural hemorrhage (differential)
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Management Protocols
Diffuse Axonal Injury (Severe)