01Approach to the Critical Patient/attcp45

Immediate stabilization

›Primary survey priorities

›Airway patency

›GCS <8 — definitive airway, rapid sequence intubation

›Apnea or irregular breathing — bag-valve-mask ventilation

›Cervical spine immobilization concurrent with airway management

›Breathing targets

›SpO2 >=94% — hypoxia worsens secondary brain injury

›PaCO2 35–40 mmHg — avoid hyperventilation except as bridge for herniation

›If herniation signs, brief hyperventilation to PaCO2 30–35 mmHg as temporizing measure

›Circulation targets

›SBP >=100 mmHg in adults — hypotension doubles mortality in TBI

›MAP 80–90 mmHg target in severe TBI with ICP monitoring

›Isotonic crystalloid resuscitation — avoid hypotonic fluids

›Hypotension from isolated TBI is rare — identify extracranial hemorrhage source

Herniation recognition and response

›Uncal herniation signs

›Ipsilateral fixed dilated pupil

›Contralateral hemiplegia (Kernohan's notch — ipsilateral hemiplegia in paradoxical cases)

›Declining GCS with Cushing's triad

›Cushing's triad components: hypertension, bradycardia, irregular respirations — late sign

›Immediate herniation management

›Mannitol 1.0 g/kg IV bolus — first-line osmotic agent

›Hypertonic saline 23.4% 30 mL IV bolus or 3% NaCl 250 mL over 30 minutes

›Elevate head of bed 30 degrees, neutral head position

›Neurosurgery emergency consultation — surgical decompression may be required

›Urgent repeat CT head

02History/hx42

Mechanism and event

›Mechanism of injury

›Falls — most common in elderly

›Motor vehicle collision — high-energy transfer

›Assault — directed blunt force

›Sports injury — helmet use, collision type

›Pedestrian struck or ejection from vehicle — high-risk mechanisms

›Event timeline

›Time of injury — TXA window is within 3 hours

›Loss of consciousness — duration, witnessed vs. unwitnessed

›Lucid interval followed by deterioration — classic "talk and die" pattern

›Post-traumatic amnesia duration — >30 minutes predicts significant intracranial injury

Symptoms

›Neurological symptoms

›Headache — severity and progression

›Vomiting — number of episodes, >1 episode is an alarm feature

›Confusion or disorientation

›Weakness or numbness — focal deficits suggest mass lesion

›Visual changes

›Speech difficulty — aphasia or dysarthria

›Seizure activity — timing, type, duration

›Other symptoms

›Rhinorrhea or otorrhea — CSF leak from basal skull fracture

›Hearing loss

›Neck pain — concurrent C-spine injury

Risk factors and context

›High-risk historical features

›Age >65 — independent predictor of contusion progression and worse outcomes

03Physical Exam/exam43

Vital signs

›Hemodynamic assessment

›Blood pressure — hypotension is rarely from isolated TBI

›Cushing's triad: hypertension + bradycardia + irregular respirations — late herniation sign

›Heart rate — tachycardia suggests extracranial hemorrhage

›Respiratory rate and pattern — Cheyne-Stokes in severe TBI

›Temperature — fever worsens secondary brain injury

›Oxygen saturation — SpO2 <94% is a critical threshold

Neurological exam

›Level of consciousness

›GCS — document E, V, M scores separately; serial reassessment mandatory

›GCS <13 — threshold for CT head in most decision rules

›GCS 3–8 — severe TBI classification

›Pupillary assessment

›Size — miosis or mydriasis

›Reactivity — unilateral fixed dilated pupil suggests uncal herniation ipsilaterally

›Quantitative pupillometry — more reliable than clinical assessment alone

›Motor exam

›Focal weakness or hemiparesis — contralateral to contusion

›Posturing — decorticate or decerebrate — severe TBI indicator

›Pronator drift

›Cranial nerves

›Extraocular movements — cranial nerve III, IV, VI

›Facial droop — cranial nerve VII

›Tongue deviation — cranial nerve XII

›Cerebellar signs

›Ataxia — posterior fossa involvement

›Nystagmus

04Differential Diagnosis/ddx38

Intracranial hemorrhage

›Epidural hematoma

›ICD-10 S06.4

›Biconvex/lenticular hyperdensity on CT

›Lucid interval followed by rapid deterioration

›Typically temporal bone fracture with middle meningeal artery injury

›Acute subdural hematoma

›ICD-10 S06.5

›Crescent-shaped collection following brain surface

›Frequently coexists with cerebral contusion

›High mortality — 50–90% in comatose patients

›Traumatic subarachnoid hemorrhage

›ICD-10 S06.6

›Blood in subarachnoid space and sulci

›Frequently accompanies contusions

›Associated with delayed vasospasm risk

Diffuse and axonal injury

›Diffuse axonal injury

›ICD-10 S06.2

›May have normal initial CT

›MRI shows petechial hemorrhages at gray-white junction

›Rotational and shearing mechanism

›Often associated with prolonged coma despite minimal CT findings

›Concussion without structural injury

›ICD-10 S06.0

›Normal CT

›Transient neurological dysfunction

›GCS typically 13–15

05Laboratory Tests/lt23

Hematologic and coagulation

›Complete blood count

›Hemoglobin — baseline for surgical planning

›Platelet count — target >100 x 10^9/L in TBI with hemorrhage

›Leukocytosis — stress response vs. infection at 48–72 hours

›Coagulation panel

›PT/INR — essential for warfarin reversal dosing; do not delay reversal for results

›aPTT — heparin or factor deficiency

›Fibrinogen — trauma-induced coagulopathy assessment

›DOAC-specific assays — anti-Xa activity for factor Xa inhibitors, thrombin time for dabigatran

›Normal DOAC-specific assays do not rule out therapeutic concentrations

›Type and screen

›All patients with significant contusion — surgical planning

Metabolic and chemistry

›Basic metabolic panel

›Sodium — hyponatremia from SIADH or cerebral salt wasting

›Glucose — hyperglycemia and hypoglycemia both worsen TBI outcomes

›Creatinine — renal function for contrast and medication dosing

›Potassium — dyskalemia with mannitol use

›Toxicology

›Blood alcohol level — intoxication impairs exam reliability

›Urine drug screen — polysubstance use affects GCS interpretation

›Additional markers

›Serum lactate — marker of systemic perfusion, target <2 mmol/l

›Liver function tests — coagulopathy, medication metabolism

06Diagnostic Tests/dt71

Scoring Systems

›Glasgow Coma Scale

›Eye opening: spontaneous (4), to voice (3), to pain (2), none (1)

›Verbal: oriented (5), confused (4), words (3), sounds (2), none (1)

›Motor: obeys (6), localizes (5), withdraws (4), flexion (3), extension (2), none (1)

›Severe TBI: GCS 3–8; moderate: GCS 9–12; mild: GCS 13–15

›Marshall CT Classification

›Diffuse injury I — no visible intracranial pathology

›Diffuse injury II — cisterns present, midline shift 0–5 mm, no mass >25 mL

›Diffuse injury III — cisterns compressed or absent, midline shift 0–5 mm

›Diffuse injury IV — midline shift >5 mm

›Evacuated mass lesion V — surgically evacuated lesion

›Non-evacuated mass lesion VI — high/mixed density >25 mL, not surgically evacuated

›Higher Marshall grade correlates with mortality and functional outcome

›Rotterdam CT Score

›Components: basal cisterns, midline shift, epidural hematoma, intraventricular or subarachnoid hemorrhage

›Scores 1–6; higher score predicts increased 6-month mortality

›Validated for prognostication in moderate to severe TBI

›Canadian CT Head Rule

›High-risk factors (neurosurgery needed): GCS <15 at 2 hours, open/depressed skull fracture, suspected basal skull fracture, vomiting >=2 times, age >=65

›Medium-risk factors (brain injury on CT): amnesia >=30 minutes, dangerous mechanism

›Applicable only to GCS 13–15 patients with LOC, amnesia, or confusion

›Sensitivity approaches 100% for clinically important brain injuries (ACEP Level B)

›PECARN TBI Rule (pediatric)

›Validated for children <18 years with GCS >=14

›Two age stratified algorithms: <2 years and >=2 years

›High-sensitivity for clinically important TBI; reduces unnecessary CT in children

CT

›Non-contrast CT head

›First-line imaging for acute TBI evaluation — gold standard

›Indications: GCS <15, focal deficit, amnesia, LOC, seizure, vomiting, dangerous mechanism

›Contusion appearance — hyperdense (hemorrhagic) or mixed-density lesions

›Classic locations — frontal and temporal poles (coup-contrecoup pattern)

›Also identifies SDH, EDH, tSAH, skull fractures, midline shift, cistern effacement

›Midline shift >5 mm and cistern effacement are strongest predictors of need for surgery

›ACR Appropriateness Criteria 2021 — usually appropriate for head trauma with high-risk features

›Repeat CT head

›GCS <=12 — repeat within 6–12 hours; contusion progression in 25–45% of cases

›Mild TBI (GCS 13–15) with small contusion <10 mL — routine repeat not required if neurologically stable

›Any neurological deterioration — immediate repeat CT

›Anticoagulated patients — lower threshold for repeat imaging

›CT cervical spine

›All high-energy mechanisms — concurrent C-spine injury

›GCS <15 — unreliable clinical clearance

›Abnormal neurological exam or neck pain with trauma

›CT angiography

›Skull base fracture involving carotid canal — carotid or vertebral artery injury risk

›Penetrating cranial injury

›Unexplained neurological deficit not explained by CT findings

MRI

›Brain MRI indications

›Not first-line in acute setting — logistical limitations

›Superior to CT for diffuse axonal injury — petechial hemorrhages at gray-white junction on gradient echo or SWI sequences

›Small contusions and posterior fossa lesions — CT can miss

›Prognostication — lesion burden and location correlate with outcome

›Subacute evaluation — within 24–72 hours when clinically stable

›MRI sequences for TBI

›T2* gradient echo — microhemorrhages, DAI

›Susceptibility weighted imaging (SWI) — most sensitive for hemorrhagic lesions

›FLAIR — edema and non-hemorrhagic contusion

›DWI — ischemic injury superimposed on trauma

›MRI limitations

›Time-intensive — not appropriate when surgical decision is pending

›Limited availability at night in many centers

›Contraindicated with certain metal implants or pacemakers

Ultrasound

›Point-of-care ultrasound

›Optic nerve sheath diameter — ONSD >5 mm associated with elevated ICP

›Sensitivity 90%, specificity 85% for ICP >20 mmHg — adjunct only, not standalone

›FAST exam — extended FAST to exclude thoracoabdominal hemorrhage in polytrauma

›Transcranial Doppler — pulsatility index as surrogate for ICP trend in monitored patients

›Ultrasound limitations

›Cannot evaluate brain parenchyma through intact skull in adults

›ONSD measurement variability between operators

›Not a substitute for CT in acute TBI evaluation

07Disposition/dispo37

ICU admission

›ICU indications

›GCS <=12 — high risk for clinical deterioration

›Contusion >10 mL or subfrontal/temporal location

›Midline shift or basal cistern effacement on CT

›Active anticoagulation or coagulopathy with intracranial hemorrhage

›Seizure activity post-injury

›ICP monitor in place

›Post-operative neurosurgical patients

›ICP monitoring indications

›GCS 3–8 after resuscitation with abnormal CT

›GCS 3–8 with normal CT plus two of: age >40, posturing, SBP <90 mmHg

Neurosurgical intervention

›Surgical consultation urgency

›All contusions on CT — neurosurgical awareness mandatory

›Urgent consultation: contusion >25 mL, midline shift, cistern effacement, declining GCS

›Immediate for herniation or rapidly expanding hematoma

›Surgical indications

›Contusion or hematoma >25 mL — consider evacuation before neurological deterioration

›Clinical deterioration plus increasing midline shift — most common surgical trigger

›Posterior fossa lesions — lower threshold for intervention given small space

›Decompressive craniectomy >=12 x 15 cm — refractory intracranial hypertension

Stepdown and observation

›Neuro-monitoring unit

›GCS 13–15 with moderate contusion or risk factors — neuro-observation appropriate

›Serial GCS and neuro checks every 1–2 hours

›Repeat CT at 6–12 hours if GCS <=12 at admission

›Observation unit

08Treatment/t90

Initial stabilization

›ATLS primary survey

›Airway — jaw thrust preferred over head tilt in trauma

›C-spine immobilization — until cleared

›Breathing — target SpO2 >=94%, PaCO2 35–40 mmHg

›Circulation — SBP >=100 mmHg; MAP 80–90 mmHg if ICP monitored

›Disability — GCS, pupils, motor

›Avoid secondary insults: hypoxia, hypotension, hyperglycemia, hyperthermia, hyponatremia

›Positioning

›Head of bed 30 degrees

›Neutral head position — avoid neck flexion or rotation that impairs venous drainage

Seizure prophylaxis

›Levetiracetam

›500–1000 mg IV/PO twice daily for 7 days

›Increasingly preferred due to fewer drug interactions and better safety profile

›Pyridoxine 50–100 mg daily may mitigate behavioral side effects

›Phenytoin alternative

›Loading dose 15–20 mg/kg IV at maximum 50 mg/min

›Maintenance 5–7 mg/kg/day in divided doses

›Monitor for cardiac arrhythmia during loading — requires cardiac monitoring

›Prophylaxis duration and scope

›7 days only — prophylaxis beyond 7 days does not prevent late post-traumatic epilepsy

›Valproic acid not recommended — associated with increased mortality compared to phenytoin

›American Academy of Neurology Practice Parameter — Level A evidence for 7-day prophylaxis

›Indicated for contusions with GCS <10, cortical contusion, depressed fracture, or early PTS

Osmotic and ICP therapy

›Mannitol

›0.25–1.0 g/kg IV bolus over 20 minutes

›Repeat every 4–6 hours as needed

›Hold if serum osmolality >320 mOsm/kg

›Contraindicated in hypovolemia — fluid resuscitate first

›Class I recommendation for elevated ICP management

›Hypertonic saline

›3% NaCl 250 mL over 30 minutes for ICP elevation

›23.4% NaCl 30 mL IV bolus for herniation

›Target serum sodium 145–155 mmol/l in refractory ICP

›Preferred over mannitol in hypotensive patients

›Tiered ICP management

›Tier 1: analgesia, sedation, head positioning, mannitol or hypertonic saline, CSF drainage

›Tier 2: neuromuscular blockade, targeted temperature management

›Tier 3: barbiturate coma, decompressive craniectomy, metabolic suppression

Anticoagulation reversal

›Warfarin reversal

›4-factor prothrombin complex concentrate (PCC) — dose based on INR and weight

›INR 2–4: 25 units/kg IV

›INR 4–6: 35 units/kg IV

›INR >6: 50 units/kg IV

›Maximum 5000 units

›IV vitamin K 10 mg concurrent — sustains reversal

›Do not delay reversal awaiting lab results in intracranial hemorrhage

›Direct oral anticoagulant reversal

›Dabigatran — idarucizumab 5 g IV (two 2.5 g vials given sequentially)

›Factor Xa inhibitors (rivaroxaban, apixaban) — andexanet alfa or 4-factor PCC 50 units/kg

›4-factor PCC is acceptable alternative when specific reversal agents unavailable

›Antiplatelet considerations

›Routine platelet transfusion for antiplatelet reversal not recommended

›Consider platelet transfusion if surgical intervention planned or ongoing hemorrhage

›Desmopressin 0.3 mcg/kg IV — may transiently improve platelet function

Tranexamic acid

›TXA evidence and use

›CRASH-3 trial: reduced head injury-related death in mild-to-moderate TBI when given within 3 hours (RR 0.78, 95% CI 0.64–0.95)

›No benefit demonstrated in severe TBI in CRASH-3

›Meta-analyses: no significant effect on overall mortality or disability; may reduce hematoma expansion; appears safe

›Data in isolated severe TBI suggest potential harm — use institution-dependent

›TXA dosing if used

›1 g IV over 10 minutes within 3 hours of injury

›Second dose 1 g IV over 8 hours if initial dose given

›Not recommended beyond 3 hours from injury

Supportive care

›Analgesia

›Acetaminophen preferred — 650–1000 mg PO/IV every 6–8 hours

›Avoid NSAIDs acutely — bleeding risk

›Opioids with caution — obscure neurological exam; use minimum effective dose

›Antiemetic therapy

›Ondansetron 4–8 mg IV every 8 hours for persistent vomiting

›Metoclopramide 10 mg IV as alternative

›Glucose management

›Target 6.1–10 mmol/l — avoid hyperglycemia >10 mmol/l and hypoglycemia

›Insulin infusion if persistent hyperglycemia in ICU patients

›Fever management

›Target normothermia — acetaminophen first-line

›Cooling blanket for refractory fever >38.5 C

›Targeted temperature management — not routine; considered in refractory ICP

›Nutrition

›NPO initially if surgical intervention possible or GCS depressed

›Early enteral nutrition within 24–72 hours — reduces mortality in severe TBI

›Avoid hypotonic fluids — risk of cerebral edema

›Isotonic feeds preferred in patients at risk for cerebral edema

›DVT prophylaxis

›Mechanical compression devices — start immediately

›Pharmacologic prophylaxis — initiate 24–72 hours post-injury if hemorrhage stable on repeat CT

Medications to avoid

›Contraindicated or high-risk agents

›Anticoagulants and antiplatelets — hold acutely

›NSAIDs — increase bleeding risk

›Excessive sedation — obscures neurological exam

›Hypotonic intravenous fluids — worsen cerebral edema

09Special Populations/sp54

Pregnancy

›Physiologic considerations

›Increased blood volume — hemorrhage may be underappreciated until decompensation

›Supine hypotension — left lateral tilt 15 degrees for >20 week gestation

›Altered drug metabolism — increased volume of distribution affects drug dosing

›Fetal monitoring — continuous electronic fetal monitoring for viable gestation after trauma

›Imaging in pregnancy

›CT head — fetal radiation dose from CT head is minimal (<1 mGy) and acceptable when clinically indicated

›MRI — preferred when time allows, no ionizing radiation

›Do not withhold CT when clinically indicated — undiagnosed intracranial injury poses greater risk than radiation

›Medications in pregnancy

›Levetiracetam — limited data; generally considered safer than phenytoin in pregnancy

›Phenytoin — FDA category D; fetal hydantoin syndrome risk with chronic use

›Mannitol — may cause fetal dehydration; use for herniation despite risks

›4-factor PCC and vitamin K — safe for anticoagulation reversal

›TXA — WOMAN trial data support use in obstetric hemorrhage; TBI data extrapolated

›Obstetric team involvement

›Immediate obstetric consultation for any significant maternal trauma

›Perimortem cesarean section if cardiac arrest at >=20 weeks gestation

Geriatric

›Epidemiology and risk

›Age >65 is an independent risk factor for contusion progression and worse outcomes

›Falls are the leading mechanism in elderly — low-energy falls can cause significant injury

›20–30% of older adults on anticoagulants or antiplatelets

›Brain atrophy — increased subdural space allows larger hematoma before symptom onset

›Higher rates of cerebrovascular comorbidity — stroke, atrophy affect baseline exam

›Modified assessment

›Lower threshold for CT — Canadian CT Head Rule has not been validated in >65 years

›Anticoagulation reversal prioritized — higher hemorrhagic complication rate

›Baseline cognitive assessment — delirium superimposed on dementia common

›Frailty and comorbidity — functional outcome prediction difficult from acute exam alone

›Treatment modifications

›Seizure prophylaxis dosing — renal clearance reduced; levetiracetam dose adjustment for eGFR <50

›Osmotic therapy — higher risk of electrolyte disturbance with mannitol and hypertonic saline

›Surgical risk stratification — higher operative mortality; goals of care discussion early

›Goals of care — advance directives, family discussion for severe TBI in older adults

›Anticoagulation restart — generally 14–90 days post-injury depending on thrombotic vs. bleeding risk

Pediatrics

›Epidemiology

›TBI is the leading cause of death and disability in children

›Falls and motor vehicle collisions most common; non-accidental trauma (NAT) in infants

›Non-accidental trauma screening — consider in <2 years with intracranial injury and inconsistent history

›Imaging decisions

›PECARN TBI decision rule — validated for children <18 years, GCS >=14

›<2 years high risk: GCS <15, palpable skull fracture, scalp hematoma (not frontal), LOC >=5 seconds, not acting normally, severe mechanism

›>=2 years high risk: GCS <15, LOC, vomiting, severe mechanism, signs of basal skull fracture

›Radiation concern — shared decision-making for low-risk PECARN category

›Physiologic differences

›Larger head-to-body ratio — increased rotational force on cervical spine

›Open fontanelles in infants — tension may indicate elevated ICP

›Hypotension threshold — SBP <70 + (2 x age in years) mmHg in children <10

›Medication dosing

›Levetiracetam — 20–40 mg/kg IV/PO twice daily; max adult dose at >50 kg

›Phenytoin — loading 20 mg/kg IV at maximum 1 mg/kg/min; monitor cardiac

›Mannitol — 0.5–1.0 g/kg IV bolus

›Hypertonic saline 3% — 2–5 mL/kg IV over 10–20 minutes

›Target ICP <20 mmHg; CPP age-dependent (>=40 mmHg infants, >=50 mmHg older children)

10Background/b59

Epidemiology

›Incidence and prevalence

›Cerebral contusion occurs in up to 8.2% of all TBI cases

›Present in 13–35% of severe TBI cases

›TBI is responsible for approximately 69 million new cases globally per year

›Leading cause of trauma-related death and disability

›In-hospital mortality for severe TBI with contusion approximately 20–30%

›Demographics and mechanism

›Bimodal age distribution — young adults (15–35) and elderly (>65)

›Males 2–3 times more likely to sustain TBI than females

›Falls are leading cause in elderly; MVA and assault in younger adults

›Alcohol intoxication present in approximately 13% of mild TBI presentations

›Lesion behavior

›Contusions are dynamic — 25–45% enlarge significantly on follow-up imaging

›Progression most likely in first 24–48 hours

›13% of patients with severe TBI were completely lucid before neurological deterioration from delayed hematoma

›Contusion/SDH/SAH cluster pattern associated with higher rates of incomplete recovery at 12 months

Pathophysiology

›Primary injury

›Direct mechanical deformation of brain parenchyma

›Coup-contrecoup pattern — frontal and temporal poles most vulnerable due to irregular skull base

›Shear forces cause axonal stretching and microvascular disruption

›Petechial hemorrhages coalesce to form macroscopic contusion

›Secondary injury cascade

›Glutamate excitotoxicity — N-methyl-D-aspartate receptor activation

›Mitochondrial dysfunction — impaired oxidative phosphorylation

›Axonal swelling — cytoskeletal disruption over hours to days

›Cerebral edema — vasogenic from blood-brain barrier disruption; cytotoxic from cellular injury

›Elevated ICP — from edema, mass effect, impaired CSF drainage

›Cerebral ischemia — CPP compromise from elevated ICP and hypotension

›Contusion expansion mechanism

›Ongoing microvascular bleeding — coagulopathy accelerates expansion

›Pericontusional edema enlarges effective mass over 24–72 hours

›Coagulopathy of TBI — traumatically injured brain releases tissue factor, activating systemic coagulation

›Lower GCS verbal score predicts larger initial contusion volume and contusion expansion

›ICD-10 classification

›S06.30 — unspecified focal traumatic brain injury

›S06.31 — contusion and laceration of right cerebrum

›S06.32 — contusion and laceration of left cerebrum

Therapeutic Considerations

›Evidence base for ICP management

›Brain Trauma Foundation (BTF) Guidelines — recommend ICP monitoring for GCS 3–8 with abnormal CT (Level IIB)

›Target ICP <22 mmHg — associated with reduced mortality in BTF guidelines

›CPP target 60–70 mmHg — avoiding aggressive CPP augmentation >70 mmHg prevents pulmonary complications

›Tiered therapy reduces secondary injury — escalate stepwise from sedation to surgery

›Surgical evidence

›Contusion evacuation >25 mL — generally accepted indication, though RCT data limited

›DECRA trial — early decompressive craniectomy reduced ICP but increased unfavorable outcomes in diffuse TBI

›RESCUEicp trial — decompressive craniectomy reduced mortality but increased vegetative state rate in refractory ICP

›Posterior fossa contusions — surgical threshold lower due to limited space and risk of rapid brainstem compression

›Anticoagulation reversal evidence

›Rapid reversal reduces hematoma expansion and improves outcomes — Level B recommendation

›4-factor PCC superior to fresh frozen plasma for speed of reversal and volume

›Idarucizumab for dabigatran — complete reversal within minutes (RE-VERSE AD trial)

›Routine platelet transfusion for antiplatelet reversal not recommended — PATCH trial showed harm

›Neuroprotection and emerging therapies

›No proven pharmacological neuroprotective agent in TBI to date

›Progesterone — failed to show benefit in PROTECT III and SyNAPSe trials

›Biomarkers — GFAP and UCH-L1 validated in FDA-cleared blood tests for mild TBI (Banyan BTI)

›S100B — used in Scandinavian guidelines to stratify CT need in mild TBI

›Restart anticoagulation 14–90 days post-TBI depending on thrombotic vs. bleeding risk balance

›Restart antiplatelet agents as early as 4 days post-injury if hemorrhage is stable

11Patient Discharge Instructions/pdi29

copy discharge instructions

›Discharge instructions for cerebral contusion

›Your injury

›You have been diagnosed with a cerebral contusion — a bruise of the brain from head injury

›This type of injury can change over the first 24–48 hours — follow-up is important

›You must not be left alone tonight — a responsible adult must stay with you

›Activity restrictions

›No driving for at least 24 hours or while taking pain medications

›No alcohol or recreational drugs — these worsen brain injury and hide important symptoms

›No return to contact sports or strenuous activity until cleared by your doctor

›Rest today — limit screen time, reading, and activities that worsen headache

›Return to school or work only when symptoms resolve and with medical guidance

›Medications

›Use acetaminophen (Tylenol) for headache — do not use ibuprofen, aspirin, or naproxen

›Take all prescribed medications including seizure medications exactly as directed

›Do not restart blood thinners without specific instructions from your doctor

›Return to emergency department immediately if

›Headache that is worsening or severe

›Vomiting more than once

›Increasing confusion, difficulty waking, or unusual drowsiness

›Weakness or numbness in arm or leg

›Seizure activity

›Clear fluid from nose or ears

›Vision changes, double vision, or slurred speech

›Unsteady walking or new falls

›Behavioral changes or agitation

›Follow-up

›Neurosurgery or neurology appointment in 2–4 weeks — call to confirm

12References/r39

Guidelines and key sources

›Brain Trauma Foundation

›Brain Trauma Foundation Guidelines for the Management of Severe TBI, 4th edition

›Provides Level IIB recommendation for ICP monitoring in GCS 3–8 with abnormal CT

›American College of Surgeons

›Best Practices in the Management of Traumatic Brain Injury, ACS 2024 (Manley et al.)

›Best Practices Guidelines in Imaging, ACS 2018 (Tominaga et al.)

›ACEP Clinical Policy

›Valente JH et al. Clinical Policy: Critical Issues in the Management of Adult Patients with Mild TBI, Ann Emerg Med 2023

›ACEP Board of Directors approval February 1, 2023; endorsed by Emergency Nurses Association

›ACR Appropriateness Criteria

›Expert Panel on Neurological Imaging, Shih RY et al. ACR Appropriateness Criteria Head Trauma: 2021 Update, J Am Coll Radiol 2021

Landmark trials

›Contusion outcomes and expansion

›Iaccarino C et al. Patients with Brain Contusions: Predictors of Outcome and Relationship Between Radiological and Clinical Evolution. J Neurosurg 2014

›Smith PD et al. Predictive Factors for Traumatic Cerebral Contusion Volume, Expansion, and Outcomes. J Neurosurg 2025

›Zhu Y et al. Establishment and Validation of Prognosis Model for Patients with Cerebral Contusion. BMC Neurol 2021

›Tranexamic acid

›CRASH-3 trial collaborators. Effects of TXA on Death, Disability, Vascular Occlusive Events in Acute TBI. Lancet 2019

›Lawati KA et al. Efficacy and Safety of TXA in Acute TBI: Systematic Review and Meta-Analysis. Intensive Care Med 2021

›Zhang M, Liu T. Efficacy and Safety of TXA in Acute TBI: Meta-Analysis of RCTs. Am J Emerg Med 2024

›Bossers SM et al. Association Between Prehospital TXA Administration and Outcomes of Severe TBI. JAMA Neurol 2021

›Anticoagulation reversal

›Maegele M et al. Coagulopathy and Haemorrhagic Progression in TBI. Lancet Neurol 2017

›Popma E et al. Reversal of Antithrombotic Medications in Patients with TBI. J Trauma Acute Care Surg 2025

›Seizure prophylaxis

›Chang BS, Lowenstein DH. Practice Parameter: Antiepileptic Drug Prophylaxis in Severe TBI. Neurology 2003

›Surgical evidence

Evidence & Review

Evidence & Review