Nervous System & Special Senses
Traumatic brain injury: severity grading and ICU management
— Bimodal age peaks: young adults (MVC, assault, sports) and elderly ≥65 (ground-level falls, often on anticoagulants).
— Falls are the #1 mechanism overall in the US; MVCs lead to death and severe TBI.
— Anticoagulated elderly with even minor head strike = high-risk cohort for delayed intracranial hemorrhage.
— Any witnessed or suspected head impact with LOC, amnesia, confusion, vomiting, seizure, or focal deficit.
— Polytrauma patient with GCS <15, unexplained hypotension/bradycardia (Cushing), or asymmetric pupils.
— Intoxicated patient with abnormal mentation — never attribute solely to alcohol until TBI excluded.
— Suspected non-accidental trauma in children (retinal hemorrhages, subdural in <2 yo).
— Mild: GCS 13–15 (concussion spectrum; ~80% of TBI).
— Moderate: GCS 9–12.
— Severe: GCS ≤8 → "GCS 8, intubate."
— Primary: irreversible mechanical damage at moment of impact.
— Secondary: preventable injury from hypoxia, hypotension, ↑ICP, hypoglycemia, hyperthermia, seizures — this is what ICU management targets.
Board pearl: A single episode of SBP <90 or SpO₂ <90% in severe TBI roughly doubles mortality — secondary insult prevention (avoid hypoxia and hypotension) drives the entire resuscitation algorithm. In Step 3 stems, the "right next step" in a severe TBI vignette is almost always airway control plus restoration of MAP/CPP before advanced imaging or neurosurgical consult.

— Transient confusion, "fog," headache, dizziness, nausea, photophobia, retrograde/anterograde amnesia.
— LOC not required; if present, typically <30 min. Post-traumatic amnesia <24 h.
— Symptoms may evolve over hours — repeat assessment essential.
— Persistent confusion, lethargy, focal deficits, vomiting, possible early seizure.
— Higher rate of intracranial lesion on CT (~40%).
— Comatose or near-comatose, posturing, pupillary asymmetry, Cushing triad (HTN + bradycardia + irregular respirations) = late herniation.
— Epidural hematoma: temporal blow, brief LOC → lucid interval → rapid deterioration. Middle meningeal artery, biconvex CT.
— Subdural hematoma: elderly, anticoagulated, fall; insidious confusion/headache over days–weeks; crescent-shaped.
— Diffuse axonal injury (DAI): high-velocity rotational MVC; coma disproportionate to CT findings.
— Contusion: coup/contrecoup, frontal/temporal poles; can blossom 24–72 h.
— Penetrating/blast: GSW, IED — high mortality, infection risk.
— Time and mechanism of injury, helmet/seatbelt, airbag deployment.
— Loss of consciousness duration, seizure activity, vomiting count.
— Anticoagulants/antiplatelets — warfarin, DOACs, clopidogrel, aspirin.
— Alcohol/drug use, prior TBI, baseline cognitive status, advance directives.
— Premorbid neuro disease (dementia, stroke) for GCS baseline.
Key distinction: Epidural = arterial bleed, lucid interval, lens-shaped, doesn't cross sutures. Subdural = venous (bridging veins), crescent-shaped, crosses sutures but not midline. On Step 3, an elderly patient on apixaban who "seemed fine after the fall" and presents 2 days later confused → SDH until proven otherwise. Always document anticoagulant timing and last dose — it changes reversal decisions and disposition cadence.

— Eye (1–4), Verbal (1–5), Motor (1–6). Motor is the strongest prognostic component.
— Document each subscore (e.g., E2V1M4 = GCS 7), not just total. Note "T" if intubated for verbal.
— Unilateral fixed, dilated pupil = uncal herniation compressing CN III → ipsilateral lesion in 90%.
— Bilateral fixed/dilated = catastrophic herniation or severe hypoxia.
— Pinpoint reactive = pontine lesion or opioid (consider naloxone trial).
— Hemiparesis (contralateral to lesion usually; Kernohan notch can flip).
— Decorticate (flexor) posturing = above red nucleus; decerebrate (extensor) = brainstem, worse prognosis.
— Aphasia, cranial nerve palsies, gaze deviation.
— Raccoon eyes (periorbital ecchymosis), Battle sign (mastoid), hemotympanum, CSF rhinorrhea/otorrhea ("halo sign" or β-2 transferrin +).
— Avoid nasogastric tube — use orogastric instead.
— CPP = MAP − ICP. Target MAP usually ≥80–90 mmHg if ICP unmeasured; CPP 60–70 mmHg when monitored.
— Hypotension in isolated TBI is rare — search for hemorrhagic source (chest, abdomen, pelvis, long bones, scalp in peds).
— Cushing reflex (HTN + bradycardia + irregular respirations) = impending herniation, NOT to be "treated" by lowering BP.
Step 3 management: In a hypotensive TBI patient, resuscitate first — give isotonic crystalloid or blood, identify bleeding source. Do NOT permit permissive hypotension in TBI even if there's hemorrhagic shock; SBP <90 is forbidden. Norepinephrine is first-line vasopressor once euvolemic to maintain CPP.

— Detects acute hemorrhage, fracture, mass effect, midline shift, herniation, hydrocephalus.
— Order in ALL moderate/severe TBI immediately after stabilization.
— Canadian CT Head Rule (adults ≥16, GCS 13–15, LOC/amnesia/confusion):
— High risk (CT mandatory): GCS <15 at 2 h, suspected open/depressed skull fx, basilar fx signs, ≥2 vomiting episodes, age ≥65.
— Medium risk: amnesia >30 min, dangerous mechanism (pedestrian struck, ejection, fall >3 ft/5 stairs).
— PECARN (pediatrics) — separate rules for <2 yo and ≥2 yo; emphasizes observation over CT in low-risk children to reduce radiation.
— New Orleans Criteria — applies to GCS 15 only; more sensitive, less specific.
— CBC, BMP, glucose (avoid hypo- and hyperglycemia), coagulation panel (PT/INR, PTT), platelets.
— Type and screen/cross for moderate–severe TBI.
— Ethanol, urine drug screen if mental status altered out of proportion.
— β-hCG in reproductive-age females before imaging/medications.
— ABG if intubated — target PaCO₂ 35–40, PaO₂ >60.
— Lactate, troponin if polytrauma; consider serum sodium baseline (anticipate SIADH/CSW/DI).
— FDA-cleared to help rule out intracranial injury in adults with mild TBI and GCS 13–15 within 12 h.
— Negative result → CT can often be avoided.
Board pearl: In an anticoagulated elderly patient with any head strike — even GCS 15, no symptoms — obtain non-contrast head CT. The pretest probability of occult ICH (and delayed bleeding) is high enough that decision rules don't apply the same way. Also check INR or DOAC level (anti-Xa for apixaban/rivaroxaban, dilute thrombin time for dabigatran).

— Indicated 6 h after initial CT for any intracranial hemorrhage to assess progression.
— Earlier if clinical deterioration (drop in GCS ≥2, new focal deficit, pupil change, refractory ↑ICP).
— Anticoagulated patients with initial negative CT — many centers obtain delayed CT at 6–24 h or extended observation; warfarin/INR >1.5 has higher delayed bleed risk than DOACs.
— Indicated for blunt cerebrovascular injury (BCVI) screening: cervical seatbelt sign, basilar/petrous skull fx, C1–C3 fx, Le Fort II/III, GCS ≤8 with no CT explanation, near-hanging.
— Modified Denver/Memphis criteria guide screening — BCVI causes stroke days later if missed.
— Superior for DAI (susceptibility-weighted imaging shows microhemorrhages), brainstem injury, small contusions.
— Used when CT findings don't explain coma, or for prognostication days into ICU course.
— Avoid in unstable patients; not first-line acute.
— Indications (BTF guidelines): severe TBI (GCS ≤8) with abnormal CT, OR normal CT plus ≥2 of: age >40, posturing, SBP <90.
— External ventricular drain (EVD) — measures ICP AND therapeutic (drains CSF). Preferred when hydrocephalus or need to drain.
— Intraparenchymal monitor (bolt) — easier placement, no drainage capacity.
— Normal ICP <22 mmHg; treat sustained ICP >22.
— Brain tissue oxygen (PbtO₂) — target >20 mmHg.
— Continuous EEG — detect non-convulsive seizures (up to 20–25% of severe TBI).
— Transcranial Doppler — vasospasm/CPP estimation.
Key distinction: CT = acute hemorrhage and surgical lesions; MRI = axonal injury, prognosis, occult lesions. On Step 3, a comatose post-MVC patient with "unremarkable CT" but persistent coma → diffuse axonal injury suspected → MRI confirms. Do not delay neurosurgical consult waiting for MRI when CT shows a surgical lesion.

— A/B — Airway: Intubate for GCS ≤8, inability to protect airway, hypoxia, agitation requiring sedation, anticipated deterioration. Use RSI with neuroprotective agents (see chunk 7). Avoid hypoxia (SpO₂ <90) and hyperventilation.
— C — Circulation: Maintain SBP ≥110 in adults 15–49 and ≥70, ≥100 in ages 50–69 (BTF). Isotonic crystalloid (NS preferred over LR to avoid hyponatremia); avoid hypotonic fluids and glucose-containing solutions.
— D — Disability: GCS, pupils, lateralizing signs, glucose.
— E — Exposure: Full trauma exam; prevent hyperthermia (worsens secondary injury).
— Mild (GCS 13–15) without ICH: Observe 4–6 h, return precautions, no acute pharmacotherapy needed beyond analgesia (avoid NSAIDs/ASA in first 24 h if any bleed risk).
— Mild with ICH or moderate: Admit for serial neuro checks q1–2 h, repeat CT at 6 h, neurosurgery consult.
— Severe: ICU admission, ICP monitor consideration, neurosurgery, advanced airway, CPP optimization.
— Tier 1: Head of bed 30°, neck midline, sedation/analgesia (propofol, fentanyl), normothermia, normocapnia, CSF drainage if EVD.
— Tier 2: Hyperosmolar therapy (3% saline bolus or mannitol), neuromuscular blockade, mild hyperventilation (PaCO₂ 30–35) as bridge only.
— Tier 3: Pentobarbital coma, decompressive craniectomy, hypothermia (controversial — not for routine ICP).
— Warfarin + ICH: 4-factor PCC (preferred over FFP) + IV vitamin K 10 mg.
— Dabigatran: idarucizumab. Apixaban/rivaroxaban: andexanet alfa or 4F-PCC.
— Antiplatelets: platelet transfusion generally NOT recommended (PATCH trial) except possibly pre-neurosurgery.
CCS pearl: In the CCS severe TBI case, order in this sequence — secure airway → IV access × 2 → isotonic fluids/blood → non-contrast head CT + C-spine CT → neurosurgery consult → ICU admit → ICP monitor → reverse anticoagulation if present → continuous EEG if comatose. Advance the clock in small intervals; recheck pupils and GCS frequently.

— Pre-treat: Fentanyl 1–3 mcg/kg to blunt sympathetic surge (avoid if hypotensive).
— Induction: Etomidate 0.3 mg/kg (hemodynamically neutral) or ketamine 1–2 mg/kg (formerly avoided due to theoretical ICP rise; now considered safe and often preferred for hypotensive TBI patients).
— Paralytic: Rocuronium 1.2 mg/kg (longer-acting, preserves later neuro exam less than succinylcholine but avoids transient ICP rise/hyperkalemia risk). Succinylcholine acceptable if no contraindications.
— Avoid propofol bolus for induction in hypotensive patients (drops MAP).
— Propofol infusion (titrate to RASS −2 to −3); watch for hypotension, propofol infusion syndrome with prolonged high-dose use.
— Fentanyl infusion for analgesia.
— Avoid benzodiazepines as first-line (delirium, prolonged ventilation); dexmedetomidine an option for lighter sedation.
— 3% hypertonic saline 250 mL bolus (or 23.4% 30 mL via central line for herniation) — preferred in hypotensive patients; target Na 145–155.
— Mannitol 0.25–1 g/kg IV bolus — osmotic diuretic; avoid if hypovolemic or renal failure. Follow serum osm (<320) and osmolar gap.
— Levetiracetam 500–1000 mg IV BID × 7 days for severe TBI, depressed skull fx, penetrating injury, cortical contusion, subdural/epidural with cortical involvement.
— Phenytoin equally effective per BTF but more drug interactions. Continue only if seizure occurs.
Board pearl: Steroids are contraindicated in TBI — the CRASH trial showed increased mortality with methylprednisolone. This is a frequent distractor on Step 3. Also: avoid prophylactic hyperventilation (PaCO₂ <30) — causes vasoconstriction and ischemia; use only as short bridge for herniation.

— Epidural hematoma: >30 mL, or >15 mm thickness, or midline shift >5 mm, or GCS ≤8 with anisocoria → emergent craniotomy/evacuation regardless of GCS.
— Acute subdural hematoma: thickness >10 mm or midline shift >5 mm on CT regardless of GCS; or GCS drop ≥2 with ICP >20 or pupillary changes.
— Intraparenchymal contusion: >50 mL, or progressive neurologic deterioration, or refractory ↑ICP.
— Posterior fossa lesions: lower threshold — small bleeds can rapidly cause brainstem compression/obstructive hydrocephalus.
— Depressed skull fracture >1 cm or open with dural penetration → elevation and washout.
— Right frontal Kocher's point; coronal suture, mid-pupillary line.
— Therapeutic (CSF drainage) and diagnostic (ICP measurement, CSF sampling).
— Complications: hemorrhage along tract, infection (ventriculitis 5–10%), malposition.
— DECRA, RESCUEicp trials: secondary/last-tier intervention for refractory ↑ICP despite maximal medical management.
— Reduces ICP and mortality but increases proportion of severely disabled survivors → shared decision-making with family.
— EVD (gold standard) vs intraparenchymal bolt (Camino, Codman).
— Calibrate at tragus (foramen of Monro level).
— Hemicraniectomy for malignant edema.
— Burr hole evacuation for chronic SDH in elderly.
— Endovascular embolization of middle meningeal artery — emerging therapy for chronic/subacute SDH to reduce recurrence.
Step 3 management: A patient with biconvex temporal hematoma, blown right pupil, and decerebrate posturing — immediate neurosurgery consult, mannitol or hypertonic saline bolus, intubate with neuroprotective RSI, hyperventilate transiently to PaCO₂ 30–35 only as bridge to OR. Do NOT delay for MRI or CTA. This is a time-critical EDH with herniation.

— Falls dominate mechanism; ground-level fall often suffices to cause significant injury due to brain atrophy stretching bridging veins.
— Higher rates of subdural hematoma, often subacute/chronic with insidious symptoms (gait change, confusion, falls).
— GCS underestimates severity in elderly — baseline cognitive impairment, polypharmacy mask deterioration.
— Anticoagulant/antiplatelet use is prevalent: ALWAYS check med list, INR, DOAC dosing/timing.
— Reverse coagulopathy aggressively even for "small" bleeds — these progress.
— Higher mortality at every GCS level; consider early goals-of-care discussion.
— Geriatric trauma protocols → trauma + geriatrics co-management improves outcomes.
— Pre-existing dementia complicates GCS assessment — use family for baseline.
— Polypharmacy review: discontinue offending meds (sedatives, anticholinergics, orthostasis-inducing antihypertensives) on discharge.
— Mannitol — avoid if CrCl <30 or AKI (worsens renal failure, causes pulmonary edema). Use hypertonic saline instead.
— LMWH (enoxaparin) for VTE prophylaxis — dose-reduce to 30 mg daily if CrCl <30, or switch to UFH 5000 U SC q8–12h.
— Levetiracetam — renally cleared; dose-adjust (e.g., 250–500 mg BID if CrCl <50).
— DOAC reversal: dabigatran is dialyzable; idarucizumab still preferred.
— Coagulopathy from cirrhosis confounds bleeding risk — check INR, fibrinogen, platelets; correct with cryoprecipitate if fibrinogen <150, platelets if <50–100.
— Avoid acetaminophen >2 g/day for analgesia in severe liver disease.
— Sedation: propofol metabolized hepatically but generally safe short-term; reduce fentanyl doses (accumulates).
— Lactulose for hepatic encephalopathy may confound mental status assessment.
Board pearl: An 80-year-old on warfarin (INR 3.2) with ground-level fall and GCS 15 has a small SDH on CT. Immediate management: 4-factor PCC + IV vitamin K, admit ICU, neurosurgery consult, repeat CT at 6 h, hold warfarin. Do NOT use FFP as first-line — slower, larger volume, less effective.

— Leading cause of pediatric death/disability; mechanisms: falls (<4 yo), MVC, sports/bicycle (school age), assault (NAT).
— Larger head:body ratio, thinner skull, open fontanelles → different injury patterns; infants can hide significant blood loss into subgaleal/intracranial space.
— Pediatric GCS modified for verbal/motor in preverbal children.
— PECARN rules identify children at very low risk of clinically important TBI who can be observed without CT — minimize radiation.
— Cushing reflex is late; tachycardia and altered mental status precede hypotension.
— Non-accidental trauma (NAT): suspect with retinal hemorrhages, posterior rib/metaphyseal fractures, multiple-stage injuries, inconsistent history, subdural in infant <2 yo. Mandatory reporting to CPS.
— Cerebral autoregulation more fragile; tighter CPP targets (age-dependent, generally 40–50 mmHg in young children).
— Hypertonic saline preferred over mannitol in pediatric ICP management.
— Maternal stabilization first — best fetal outcome = best maternal outcome.
— Don't withhold head CT for clinically indicated imaging; abdominal shielding minimizes fetal dose (head CT exposes fetus to <0.01 mGy).
— Left lateral tilt (15°) after 20 weeks to relieve aortocaval compression.
— Consider Kleihauer-Betke test in Rh-negative mothers with abdominal trauma; RhoGAM if indicated.
— Phenytoin teratogenic — levetiracetam preferred for seizure prophylaxis.
— Mannitol crosses placenta — can cause fetal dehydration; use hypertonic saline preferentially.
— Continuous fetal monitoring if ≥23 weeks for at least 4–6 h after trauma; longer if contractions, bleeding, or abnormal tracing.
— Perimortem C-section within 4 min of maternal arrest if ≥23 weeks.
Key distinction: In pediatric vs adult TBI, secondary injury prevention is even more critical because pediatric brains have better recovery potential if hypoxia/hypotension/hyperthermia are prevented. Hypotension in pediatric TBI is defined by age-specific SBP (e.g., <70 + 2×age for children 1–10 yr); a "normal" adult-style SBP of 90 in a 4-year-old is shock.

— Herniation syndromes: uncal (CN III palsy, contralateral hemiparesis), central (Cushing, decerebrate posturing), tonsillar (apnea, death), subfalcine (ACA stroke).
— Post-traumatic seizures: early (<7 days) — provoked, prophylaxis with LEV × 7 days; late (>7 days) — epilepsy risk 10–25%, treat as new-onset epilepsy.
— Hydrocephalus: communicating (post-SAH/blood blocking arachnoid villi) or obstructive; may need permanent VP shunt.
— Cerebral vasospasm (post-traumatic SAH) — peak days 4–14; monitor with TCD.
— Blunt cerebrovascular injury (BCVI): carotid/vertebral dissection → delayed stroke; treat with antiplatelet/anticoagulation.
— Neurogenic pulmonary edema — sudden, sympathetic surge; treat with supportive ventilation.
— Cardiac dysfunction: stress (takotsubo) cardiomyopathy, arrhythmias, troponin elevation.
— Coagulopathy of TBI — release of tissue factor; correlates with worse outcomes.
— VTE: very high risk (30–40% without prophylaxis); balance with bleed risk for chemoprophylaxis timing.
— Ventilator-associated pneumonia, central line infections, catheter-associated UTI — bundle prevention.
— Critical illness myopathy/neuropathy.
— Diabetes insipidus (central) — hypernatremia, polyuria, low urine osm → desmopressin.
— SIADH — hyponatremia, concentrated urine → fluid restriction (cautiously; CPP).
— Cerebral salt wasting — hyponatremia with volume depletion → hypertonic saline + salt.
— Hypopituitarism — chronic; screen survivors at 3–6 months.
— Post-concussive syndrome — headache, dizziness, cognitive/mood symptoms.
— Chronic traumatic encephalopathy (CTE) — repetitive subconcussive injury.
— Cognitive deficits, depression, PTSD, behavioral changes, sleep disorders.
Board pearl: Distinguishing SIADH from cerebral salt wasting in TBI hinges on volume status: SIADH = euvolemic/hypervolemic → restrict fluids. CSW = hypovolemic → give salt + volume. Restricting fluids in CSW worsens cerebral perfusion — a classic Step 3 trap.

— All severe TBI (GCS ≤8) regardless of CT findings.
— Moderate TBI (GCS 9–12) with abnormal CT or clinical instability.
— Mild TBI with any intracranial hemorrhage or skull fracture.
— Need for ICP monitoring, ventilator, hyperosmolar therapy, or close neuro checks (q1h).
— Anticoagulated patient post-reversal with ICH.
— Post-craniotomy/craniectomy.
— Any acute intracranial hemorrhage on CT.
— Skull fracture (especially depressed, basilar, open).
— GCS ≤12, focal deficit, pupillary asymmetry.
— Worsening exam regardless of initial imaging.
— Mild TBI with isolated small SDH/contusion, stable repeat CT at 6 h, GCS 15, no anticoagulation, reliable neuro exam.
— Concussion with persistent vomiting or symptoms needing observation.
— Normal CT or negative validated decision rule.
— Symptoms improving, tolerating PO, ambulating safely.
— Sober, reliable caregiver, return precautions reviewed.
— Not on anticoagulation (or appropriately observed if so).
— Any moderate/severe TBI at facility without neurosurgery 24/7.
— Pediatric TBI to pediatric trauma center when possible.
— Penetrating TBI, depressed/open skull fx.
— Do NOT delay transfer for non-essential workup; "scoop and run" with airway/CPP support.
Step 3 management: A community ED has a GCS 6 patient with large SDH and 8 mm midline shift, no neurosurgeon on call. Action: intubate with neuroprotective RSI, mannitol or 3% saline, elevate HOB 30°, call air transport to nearest level I trauma center, send CT images electronically with patient. Do NOT keep patient for further imaging.

— Arterial (middle meningeal artery typical), temporal bone fracture, biconvex/lentiform shape, doesn't cross sutures.
— Classic "lucid interval" then deterioration. Surgical emergency if >30 mL or symptomatic.
— Venous (bridging veins), crescent-shaped, crosses sutures but not midline.
— Higher mortality than EDH due to associated parenchymal injury.
— Elderly, anticoagulated, alcoholic patients overrepresented.
— Weeks–months after minor or forgotten trauma; hypodense or mixed-density on CT.
— Elderly with insidious cognitive decline, gait disturbance, headache — mimics dementia/NPH.
— Burr hole drainage or MMA embolization.
— Blood in sulci, basal cisterns; less likely to cause vasospasm than aneurysmal SAH but possible.
— Often coexists with other injuries; usually managed conservatively.
— Coup/contrecoup, frontal/temporal poles most common.
— Can "blossom" 24–72 h — repeat CT mandatory.
— High-velocity rotational/shear forces; coma disproportionate to CT.
— MRI SWI shows punctate hemorrhages at gray-white junction, corpus callosum, brainstem.
— Poor prognosis with brainstem involvement.
— Linear (most common), depressed (surgical if >1 cm), basilar (CSF leak, cranial nerve injury), open (infection risk).
— GSW, stab; high mortality, especially bihemispheric or transventricular trajectory.
Key distinction: EDH = lens-shaped, doesn't cross sutures, often arterial, classic lucid interval. SDH = crescent-shaped, crosses sutures but not midline, venous, elderly/anticoagulated. tSAH = blood in sulci, usually managed medically. Memorizing these three CT shapes is virtually guaranteed on Step 3 imaging questions.

— Aneurysmal SAH: thunderclap headache, blood in basal cisterns, "worst headache of life" — CT angiography or LP (xanthochromia).
— Hypertensive ICH: basal ganglia, thalamus, pons, cerebellum; long-standing HTN.
— AVM rupture: younger patients, lobar bleeds.
— Amyloid angiopathy: lobar bleeds in elderly, recurrent.
— Always consider whether the head strike was the cause or the result of an event.
— Get ECG, troponin, glucose, CT/CTA, consider neurologic etiology of fall.
— Tongue laceration, urinary incontinence, post-ictal confusion.
— May have head strike during seizure → both processes simultaneously.
— Confusion, altered mental status mimicking TBI; check glucose, electrolytes, ammonia, toxicology.
— Meningitis, encephalitis — fever, meningismus, headache; rare to confuse with trauma but consider in elderly fall patient with fever.
— Spontaneous bleed into glioma, melanoma metastasis, renal cell metastasis; atypical location/edema pattern on CT/MRI.
— Atypical presentations of altered mental status, headache, seizure.
— Arrhythmia, aortic stenosis, vasovagal — workup with ECG, echo, telemetry.
Step 3 management: Elderly patient "found down" with bruise on head and small SDH on CT. Don't stop at "trauma" — workup the cause of the fall: orthostatics, ECG (arrhythmia, MI), glucose, electrolytes, medication review (antihypertensives, sedatives), and consider syncope evaluation. Treating only the SDH and discharging without identifying recurrent fall risk is a Step 3 patient-safety failure.

— Acetaminophen first-line for headache; avoid NSAIDs/ASA × 24–48 h if any bleed risk.
— Antiemetics (ondansetron) PRN for nausea.
— Resume home medications cautiously; reconcile carefully.
— Hold anticoagulation after ICH; restart timing individualized — typically 1–4 weeks for high-thrombotic-risk patients (mechanical valve, recent VTE), 4–8 weeks otherwise.
— Multidisciplinary discussion: neurology/neurosurgery, cardiology, hematology.
— DOACs generally preferred over warfarin when restarting (lower ICH recurrence).
— Antiplatelets for primary prevention often permanently discontinued; secondary prevention (post-MI, stroke) usually resumed at 1–2 weeks.
— Continue levetiracetam only if seizure occurred or high-risk (penetrating injury, depressed skull fx with cortical injury).
— Routine post-TBI prophylaxis beyond 7 days NOT indicated — doesn't prevent late epilepsy.
— Home safety eval (remove rugs, lighting, grab bars), PT/OT referral.
— Vision exam, medication review (deprescribe sedatives, anticholinergics).
— Vitamin D + calcium; bone density evaluation.
— Driving evaluation if cognitive or motor deficits.
— Concussion: stepwise return-to-play (RTP) over ~7 days; symptom-limited; no same-day RTP after concussion (sports concussion guidelines).
— Return-to-learn (school) often precedes return-to-play.
— Driving restrictions — no driving until cleared, particularly with seizure or visual deficit (state-specific reporting laws).
Board pearl: After a single concussion, return to play is graded over a minimum of 6 stages with 24 h between stages, only progressing if asymptomatic. Second-impact syndrome — catastrophic cerebral edema from a second concussion before the first resolves — is rare but devastating and the rationale for strict RTP rules in adolescent athletes.

— PCP or sports medicine follow-up in 1–2 weeks; sooner if symptomatic.
— Persistent post-concussive symptoms (>4 weeks adults, >2 weeks children) → refer to concussion clinic, neurology, or neuropsychology.
— Validated tools: SCAT5 (Sport Concussion Assessment), Rivermead Post-Concussion Symptoms Questionnaire.
— Neurosurgery 2–4 weeks for imaging review and incision/EVD site check.
— Neurology for seizure management, cognitive evaluation.
— Physical medicine & rehabilitation (PM&R) early — inpatient acute rehab when medically stable.
— Speech/language pathology, OT, PT, neuropsychology.
— Glasgow Outcome Scale–Extended (GOS-E).
— Disability Rating Scale, FIM (Functional Independence Measure).
— Screen for hypopituitarism at 3 and 12 months post-severe TBI (fatigue, weight changes, sexual dysfunction → check IGF-1, cortisol, TSH/free T4, gonadotropins, prolactin).
— Depression, anxiety, PTSD common — PHQ-9, GAD-7 screening at follow-ups.
— Substance use screening.
— Suicide risk elevated post-TBI; ask directly.
— Routine repeat imaging not needed after small stable bleeds; clinical-driven.
— Chronic SDH may need follow-up imaging if symptoms recur.
— Cognitive demands assessed; gradual reintegration.
— Vocational rehabilitation referral for adult survivors with persistent deficits.
Step 3 management: For a patient discharged after moderate TBI, set up a multidisciplinary cadence: PCP at 1 week, neurosurgery at 2–4 weeks, PM&R/rehab initiated before discharge, neuropsych testing at 4–6 weeks, endocrine screen at 3 months, mental health screen at every visit. This bundled longitudinal plan is the Step 3 "right answer" for chronic TBI management.

— Severe TBI patients lack capacity → surrogate decision-maker (advance directive > spouse > adult children > parents > siblings, per most state hierarchies).
— Emergency exception (implied consent) for life-saving interventions in unconscious patients.
— Document capacity assessments serially as patients recover.
— Avoid premature withdrawal of life-sustaining therapy ("self-fulfilling prophecy") — prognostic models (IMPACT, CRASH) inform but don't dictate; wait 72 h minimum, often longer.
— Family meetings early and repeatedly; involve palliative care.
— Brain death determination per institutional protocol if applicable (apnea test, ancillary testing).
— Decoupled from goals-of-care discussion; involve organ procurement organization (OPO) per federal law before any conversation with family about donation.
— Suspected child abuse/NAT: mandatory to CPS in all states — concrete Step 3 trigger.
— Elder abuse: mandatory in most states.
— Intimate partner violence: state-specific; some require, most encourage.
— Gunshot/stab wounds: mandatory law enforcement reporting in most states.
— Impaired driving (seizure, dementia post-TBI): state-specific DMV reporting (e.g., California mandatory; others voluntary).
— Medication reconciliation at every transition (ED → ICU → floor → rehab → home) — anticoagulants, antiepileptics, antihypertensives are the highest-risk meds.
— Clear documentation of when/whether to restart anticoagulation, with named responsible clinician and follow-up date.
— Closed-loop communication with PCP within 48 h of discharge.
— Written discharge instructions in patient's language and reading level; verify understanding (teach-back).
— Reliable caregiver to monitor for 24 h with specific red flags (worsening headache, vomiting, confusion, weakness, seizure).
Board pearl: Concrete Step 3 trigger — an infant with subdural hematoma, retinal hemorrhages, and inconsistent history → mandatory CPS report before discharge, regardless of family's wishes; admit for safety and protective workup. Failure to report is both clinically and legally indefensible.

Key distinction: A "GCS 13" mild TBI patient with abnormal CT is managed like a moderate TBI — admit, serial neuro checks, neurosurgery consult, repeat CT. The number alone doesn't dictate disposition; CT findings + anticoagulation status + age do.

— Answer: emergent craniotomy; CT shows biconvex temporal hematoma. Intubate first, mannitol or 3% saline bridge.
— Answer: 4-factor PCC + IV vitamin K, admit ICU, neurosurgery consult, repeat CT at 6 h.
— Answer: resuscitate with isotonic fluid/blood to SBP >110, then norepinephrine for CPP 60–70; ICP monitor, hypertonic saline; AVOID steroids; AVOID prophylactic hyperventilation.
— Answer: mandatory CPS report, admit, skeletal survey, ophthalmology, social work.
— Answer: MRI brain (SWI shows microhemorrhages) confirms DAI; supportive ICU management, prognosis guarded.
— Answer: do NOT lower BP — sign of impending herniation. Hypertonic saline/mannitol, hyperventilate as bridge, emergent neurosurgery.
— Answer: stepwise RTP protocol, must remain asymptomatic through graduated stages with ≥24 h between, full RTP only after final asymptomatic stage.
Step 3 management: Recognize the mechanism + CT pattern + anticoagulation status + GCS trajectory as the four data points that drive disposition and pharmacotherapy. The exam rewards systematic resuscitation order over esoteric details.

Traumatic brain injury management hinges on preventing secondary injury — secure the airway when GCS ≤8, maintain SBP and CPP, image with non-contrast CT, reverse anticoagulation urgently, escalate to ICU with neurosurgery for any acute intracranial hemorrhage, and stratify long-term care by severity with structured follow-up for cognitive, endocrine, and mental health sequelae.
Board pearl: The single most tested principle in Step 3 TBI questions is secondary injury prevention — every "next best step" answer in a severe TBI vignette involves restoring oxygenation, perfusion, and CPP before pursuing definitive diagnostics or specialty interventions. Master that order, and the rest of the topic falls into place.

