ABPN Neurocritical Care cheat sheet

Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) minus intracranial pressure (ICP); typical adult target 60-70 mmHg.

Monro-Kellie doctrine: intracranial volume is fixed (brain, blood, CSF), so an expanding mass first displaces CSF and venous blood before ICP rises steeply.

Cerebral blood flow is ~50 mL/100 g/min; flow is pressure-passive below MAP ~60 mmHg and above ~150 mmHg.

CBF varies directly with PaCO2 (~3-4% per mmHg change) and is minimally affected by PaO2 until PaO2 falls below ~50 mmHg.

Cerebral autoregulation is lost in ischemia, trauma, and severe acidosis; CBF becomes pressure-dependent.

ICP waveform: P1 (percussive, arterial), P2 (tidal, compliance), P3 (dicrotic); loss of P2 < P1 and rising P2 indicate falling compliance.

Normal ICP is 5-15 mmHg in adults; sustained ICP >20-22 mmHg is the usual treatment threshold.

Brain tissue oxygen (PbtO2) normal is 23-35 mmHg; values <15-20 mmHg indicate risk of ischemic injury.

Jugular venous bulb oximetry: SjvO2 <50% suggests ischemia; >75% suggests hyperemia or infarcted tissue.

IV thrombolysis (alteplase 0.9 mg/kg, max 90 mg) is approved within 4.5 h of ischemic stroke onset; tenecteplase 0.25 mg/kg is an accepted alternative.

Mechanical thrombectomy is indicated for large vessel occlusion up to 24 h in selected patients using DAWN/DEFUSE-3 imaging criteria.

Blood pressure after IV thrombolysis: keep <180/105 mmHg for 24 h; after successful thrombectomy, avoid hypotension and typically target <180/105 mmHg.

Hemorrhagic transformation risk rises with large infarct, hyperglycemia, and uncontrolled hypertension.

Aneurysmal subarachnoid hemorrhage: nimodipine 60 mg PO q4h for 21 days reduces delayed cerebral ischemia and poor outcome.

SAH vasospasm peaks days 3-14; monitor with transcranial Doppler (mean flow velocity >120 cm/s in MCA suggests vasospasm).

Reversible cerebral vasoconstriction syndrome presents with thunderclap headache and segmental arterial narrowing; often triggers include serotonergic drugs and postpartum state.

Cerebral venous sinus thrombosis: anticoagulation with heparin/LMWH is first-line even with hemorrhagic venous infarction.

ICH: systolic BP target 130-150 mmHg is reasonable; reverse anticoagulation urgently (e.g., vitamin K plus 4F-PCC for warfarin).

TBI: avoid hypoxia (SpO2 <90%) and hypotension (SBP <100-110 mmHg); each episode worsens outcome.

Hyperosmolar therapy: mannitol 0.5-1 g/kg or hypertonic saline (3% bolus 150-250 mL); target serum Na and osmolality per protocol.

Brief hyperventilation to PaCO2 30-35 mmHg is a temporizing bridge for impending herniation only.

Prophylactic phenytoin/levetiracetam for 7 days reduces early post-traumatic seizures; it does not prevent late epilepsy.

Therapeutic hypothermia and decompressive craniectomy are not routine for all severe TBI; craniectomy is considered for refractory ICP elevation.

Spinal cord injury: maintain MAP 85-90 mmHg for 5-7 days to support cord perfusion.

High cervical injury impairs diaphragm function (C3-C5); monitor for respiratory failure and neurogenic shock.

Neurogenic shock: hypotension with bradycardia from loss of sympathetic tone; treat with vasopressors and atropine for bradycardia.

Steroids are not recommended in acute traumatic spinal cord injury (harm with high-dose methylprednisolone).

Status epilepticus: benzodiazepine first-line (lorazepam 0.1 mg/kg IV, max 4 mg; may repeat once), then second-line antiseizure medication.

Second-line options: levetiracetam 60 mg/kg (max 4500 mg), fosphenytoin 20 PE/kg, or valproate 40 mg/kg.

Refractory status epilepticus: continuous IV anesthetic (midazolam, propofol, or pentobarbital) titrated to EEG burst suppression.

Nonconvulsive status epilepticus should be suspected in unexplained persistent coma; obtain urgent continuous EEG.

Generalized convulsive status epilepticus lasting >30 min carries risk of rhabdomyolysis, hyperthermia, and excitotoxic injury.

Propofol infusion syndrome: metabolic acidosis, rhabdomyolysis, bradycardia, and cardiac failure with prolonged high-dose infusion.

EEG burst suppression typically targets 1-3 bursts per second or isoelectric periods of several seconds.

Postanoxic myoclonus and generalized periodic discharges after cardiac arrest are poor prognostic features.

Continuous EEG should be started within 1 h in suspected nonconvulsive status and continued for at least 24 h.

Guillain-Barre syndrome: IVIG 0.4 g/kg/day for 5 days or plasma exchange; corticosteroids are not effective.

GBS respiratory failure: intubate for vital capacity <15-20 mL/kg, declining trend, or bulbar dysfunction.

Myasthenic crisis: treat with plasma exchange or IVIG; avoid aminoglycosides, magnesium, and quinolones that worsen weakness.

ICU-acquired weakness: consider after 5-7 days of critical illness; diagnosis by clinical exam and EMG/NCS.

Bacterial meningitis: dexamethasone 0.15 mg/kg q6h before or with first antibiotic dose in adults with suspected pneumococcal disease.

Empiric meningitis therapy in adults: vancomycin plus ceftriaxone (plus ampicillin if Listeria risk).

HSV encephalitis: IV acyclovir 10 mg/kg q8h for 14-21 days; do not delay for CSF PCR result.

CSF findings: bacterial (neutrophilic, low glucose, high protein), viral (lymphocytic, normal glucose), TB/fungal (lymphocytic, low glucose).

Tetanus and botulism cause descending (botulism) or trismus-predominant (tetanus) neuromuscular blockade; treat with antitoxin and supportive care.

After craniotomy, monitor for postoperative hematoma, seizures, and cerebral edema; routine prophylactic antiseizure drugs are not universally indicated.

Postoperative hyponatremia after transsphenoidal surgery often reflects SIADH or cerebral salt wasting; distinguish by volume status.

Cerebral salt wasting: hypovolemia with high urine sodium and low serum sodium; treat with volume and salt replacement.

SIADH: euvolemia with concentrated urine and low serum sodium; treat with fluid restriction.

CSF leak: suspect with clear rhinorrhea; confirm with beta-2 transferrin; avoid positive pressure and Valsalva.

After posterior fossa surgery, monitor for hydrocephalus and brainstem compression; keep head elevated 15-30 degrees.

Postoperative pituitary apoplexy or hypopituitarism requires stress-dose hydrocortisone before thyroid replacement.

Deep brain stimulation and other implanted hardware: avoid MRI outside approved conditions and unipolar electrocautery near leads.

Neurosurgical patients on dexamethasone require glucose monitoring and GI prophylaxis consideration.

Neurocritical patients are at high risk for ventilator-associated pneumonia; elevate head of bed 30 degrees unless contraindicated.

Acute respiratory distress syndrome: low tidal volume 6 mL/kg predicted body weight and plateau pressure <30 cmH2O.

Hypernatremia correction should not exceed 10-12 mEq/L per day to avoid cerebral edema.

Hyponatremia correction should not exceed 8-10 mEq/L per day to avoid osmotic demyelination.

Stress cardiomyopathy (Takotsubo) and neurogenic pulmonary edema can follow SAH and severe TBI.

Fever increases cerebral metabolic demand; treat core temperature >38 C aggressively in brain-injured patients.

Target normoglycemia (typically 140-180 mg/dL) to avoid hypoglycemia-related neuronal injury.

Vasopressors: norepinephrine is first-line for neurogenic shock; avoid excessive pressors that worsen pulmonary edema.

VTE prophylaxis with mechanical devices early; pharmacologic prophylaxis once bleeding risk is acceptable.

CT hyperdense MCA sign indicates acute thrombus; loss of gray-white differentiation and insular ribbon sign are early ischemic changes.

ASPECTS score: 10-point CT scoring system; lower scores indicate larger established infarction.

MRI DWI is most sensitive for acute ischemia within minutes; ADC maps confirm restricted diffusion.

Transcranial Doppler: MCA mean flow velocity >120 cm/s suggests vasospasm; Lindegaard ratio >3 supports it.

Pupillometry and automated pupillometry provide objective assessment of brainstem function.

Brain death requires coma, absent brainstem reflexes, and apnea in the setting of a known cause and adequate MAP.

Apnea test: disconnect ventilator, deliver 100% O2 via catheter; positive if no respiratory effort with PaCO2 >=60 mmHg (or 20 mmHg rise).

Ancillary tests for brain death include EEG (electrocerebral silence), cerebral angiography (no flow), and radionuclide perfusion.

Confounders for brain death exam: hypothermia, sedatives/neuromuscular blockers, severe metabolic derangement.

Prognostication after cardiac arrest should use multimodal assessment: exam, EEG, SSEP, biomarker, and imaging at >=72 h.

Bilateral absence of N20 on median nerve SSEP is a strong predictor of poor outcome after anoxic injury.

Absent pupillary and corneal reflexes at 72 h after cardiac arrest predict poor neurologic outcome.

Withdrawal of life-sustaining therapy decisions should follow surrogate decision-making standards and documented patient values.

Brain death declaration requires two independent exams per institutional protocol and exclusion of confounders.

Organ donation after circulatory death (DCD) and brain death (DBD) require separate protocols and consent processes.

Palliative care consultation improves symptom control and family satisfaction in neurocritical illness.

Do-not-resuscitate orders do not preclude other treatments; clarify goals-of-care separately.

Ethical principles: autonomy, beneficence, nonmaleficence, and justice guide allocation of scarce ICU resources.

Naloxone reverses opioid-induced respiratory depression; titrate to respiratory effort, not full arousal.

Flumazenil reverses benzodiazepines but can precipitate seizures in mixed overdose or chronic benzodiazepine use.

Physostigmine can reverse anticholinergic delirium but risks seizures and bradycardia.

Toxic alcohol (methanol, ethylene glycol) poisoning: treat with fomepizole or ethanol; consider hemodialysis.

Serotonin syndrome: clonus, hyperthermia, autonomic instability; treat with cyproheptadine and supportive care.

Neuroleptic malignant syndrome: rigidity, hyperthermia, elevated CK; treat with dantrolene or bromocriptine.

Phenytoin toxicity causes nystagmus, ataxia, and confusion; monitor free levels in hypoalbuminemia.

Carbamazepine and oxcarbazepine can cause hyponatremia via SIADH.

Valproate causes hyperammonemia and hepatotoxicity; avoid in urea cycle disorders.