Free ABIM Neurocritical Care Exam Flashcards

Pupillary size/reactivity, brainstem reflexes (corneal, oculocephalic, cough), and motor asymmetry. GCS cannot be verbally scored in sedated or intubated patients, so document best eye/motor response, note sedation status, and track trend over time rather than a single score.

Brain, blood, and CSF volumes sum to a fixed intracranial volume. A growing mass (hematoma, edema) is first compensated by displacing CSF and venous blood; once that reserve is exhausted, small further volume increases cause steep, nonlinear ICP rises.

Normally, cerebral blood flow stays roughly constant across a wide MAP range through vessel tone changes. Autoregulation is often impaired in injured brain, so CBF then tracks MAP passively - abrupt BP swings can directly cause ischemia or hyperemia/edema.

Mannitol (0.25-1 g/kg IV bolus) draws water from brain into plasma by osmotic gradient and causes an osmotic diuresis. Monitor volume status, renal function, sodium, and the osmolar gap; NCS 2020 prefers the osmolar gap over a fixed serum-osmolality cutoff, and the traditional 320 mOsm/kg ceiling is not evidence-based.

Hypertonic saline (e.g., 3% bolus) raises serum sodium to draw free water out of brain tissue without mannitol's osmotic diuresis, so it avoids worsening hypovolemia or hypotension - useful in unstable, hyponatremic, or volume-depleted patients.

4-factor prothrombin complex concentrate (dosed by INR and weight) corrects the coagulopathy within minutes, given together with IV vitamin K, which is required because 4F-PCC's factor correction is transient and vitamin K sustains it.

Idarucizumab, a monoclonal antibody fragment that binds dabigatran directly, is given as two consecutive 2.5 g IV infusions (5 g total), producing reversal within minutes. It has no effect on factor Xa inhibitors.

Give 4-factor PCC (off-label; the 2022 AHA/ASA ICH guideline rates it COR 2b). Andexxa left the US market on December 22, 2025, after FDA judged its thromboembolic risks outweighed its benefits; in ANNEXA-I (NEJM 2024) it improved hemostasis but raised thrombotic events (10.3% vs 5.6%).

Its short half-life allows rapid wake-up for serial neuro exams, and it lowers cerebral metabolic rate/ICP. Prolonged high-dose infusions risk propofol infusion syndrome (metabolic acidosis, rhabdomyolysis, cardiac failure) - monitor triglycerides and CK.

ESETT (2019) found IV fosphenytoin, valproate, and levetiracetam roughly equally effective (about 45-47% seizure cessation) for benzodiazepine-refractory status epilepticus, with similar safety - agent choice can be guided by comorbidities rather than presumed superiority.

Not shown to. SETPOINT2 (JAMA 2022) randomized 382 ventilated severe-stroke patients to tracheostomy within 5 days or to weaning with tracheostomy from day 10 if needed. Survival without severe disability (mRS 0–4) at 6 months was 43.5% vs 47.1% (not significant), with no difference in ventilation duration or ICU stay.

Target normocapnia (PaCO2 roughly 35-40 mmHg) and the lowest PEEP that maintains oxygenation. High PEEP can impede cerebral venous outflow and modestly raise ICP; hypercapnia raises CBF/ICP, and hypoxia worsens secondary injury.

Overall neurologic complications and ischemic stroke are more common with VA-ECMO; intracranial hemorrhage is not (ELSO registry: about 1.8% on VA vs 3.6% on VV). Anticoagulation drives ICH on either mode, so use serial neuro exams and a low threshold for imaging.

Neurogenic shock (from cervical/high-thoracic spinal cord injury) causes hypotension WITH bradycardia, from loss of sympathetic tone and unopposed vagal input - unlike hypovolemic or septic shock, which cause reflex tachycardia. Treat with vasopressors supporting both tone and rate.

Start within 24-48 hours once hemodynamically stable. Severe TBI causes a hypermetabolic, catabolic state; BTF recommends reaching basal caloric replacement by day 5, and no later than day 7, post-injury to reduce mortality. A post-pyloric route is considered if gastric residuals are high.

Fever raises cerebral metabolic demand and can worsen secondary injury and ICP. Treat fever to normothermia and find its source; after cardiac arrest, actively prevent fever. In normothermic acute ischemic stroke, prophylactic fever prevention or induced hypothermia is not recommended (2026 AHA/ASA, COR 3: No Benefit).

Mechanical prophylaxis (intermittent pneumatic compression) starts immediately. Pharmacologic prophylaxis (e.g., subcutaneous heparin) is generally added once hematoma stability is confirmed on repeat imaging, commonly 24-48 hours after onset, balancing VTE risk against rebleeding risk.

Delirium is an acute, fluctuating disturbance of attention and awareness with an identifiable precipitant (sedation, infection, metabolic derangement), unlike dementia's chronic stable decline. Validated tools (e.g., CAM-ICU) should be used routinely, since delirium is frequently missed by gestalt exam.

A catecholamine surge raises pulmonary capillary pressure and vascular permeability, causing rapid-onset pulmonary edema without primary cardiac or renal failure. It typically improves within 48-72 hours with supportive respiratory care once the neurologic insult is controlled.

Neurogenic (Takotsubo-like) stress cardiomyopathy from catecholamine surge, causing troponin elevation, ECG changes, and reduced ejection fraction. After SAH it often follows a basal/mid-ventricular 'reverse Takotsubo' pattern rather than classic apical ballooning; normal coronaries on angiography confirm it, and it is usually reversible over days to weeks.

DI: high sodium, hypovolemic, dilute polyuria. SIADH: low sodium, euvolemic, concentrated urine. Cerebral salt wasting: low sodium, hypovolemic, high urine sodium - volume status is the key discriminator between SIADH and CSW, both common after SAH/TBI.

No. Whether hyponatremia is from SIADH or cerebral salt wasting, fluid restriction after aSAH raises the risk of delayed cerebral ischemia. Maintain euvolemia and replete sodium and volume losses instead; assess volume status directly rather than restricting fluids based on sodium level alone.

New thrombocytopenia with microangiopathic hemolytic anemia (schistocytes) plus altered mental status or focal deficits. TTP is a hematologic emergency treated with urgent plasma exchange; platelet transfusion is generally avoided unless there is life-threatening bleeding, since it can worsen microthrombosis.

Automated CT or MR perfusion showing salvageable penumbra supports IVT 4.5-9 hours after last known well, or on waking within 9 hours of the sleep midpoint (2026 AHA/ASA, COR 2a). An MRI DWI-FLAIR mismatch supports IVT within 4.5 hours of symptom recognition for unknown-onset stroke.

Patients with persistently altered or unexplained mental status - especially after a convulsive seizure without return to baseline, or comatose post-arrest patients. Nonconvulsive seizures and nonconvulsive status epilepticus are common and are missed without cEEG, generally for at least 24-48 hours.

An EVD measures ICP AND allows therapeutic CSF drainage - the reference standard - but carries higher infection/hemorrhage risk from ventricular cannulation. A parenchymal monitor is easier to place with lower complication rates but cannot drain CSF.

Elevated middle cerebral artery mean flow velocity plus a Lindegaard ratio (MCA velocity divided by extracranial ICA velocity) above 3 suggests vasospasm; a ratio above 6 suggests severe vasospasm rather than hyperemia, which also raises MCA velocity.

They detect regional or global cerebral ischemia even when ICP is normal. A PbtO2 below roughly 20 mmHg or SjvO2 below 50-55% signals inadequate oxygen delivery relative to demand, prompting optimization of CPP, oxygenation, or sedation.

An established, irreversible cause of catastrophic brain injury; exclusion of confounders (sedating or paralytic drugs, severe metabolic/endocrine derangement, hypothermia); and, in adults, SBP of at least 100 mmHg and MAP of at least 75 mmHg with a core temperature of at least 36°C (2023 AAN/AAP/CNS/SCCM consensus guideline).

No respiratory effort, arterial pH below 7.30, and PaCO2 of at least 60 mmHg AND at least 20 mmHg above the pre-test baseline (2023 AAN/AAP/CNS/SCCM guideline). Abort for any breath, SBP below 100 or MAP below 75 mmHg, or SpO2 falling below 85%.

Deliberate temperature control at a constant target of 32-37.5°C (2025 AHA, COR 1), maintained for at least 36 hours in total (COR 2a). TTM2 found 33°C no better than normothermia with fever prevention (≤37.5°C); ERC-ESICM 2025 advises actively preventing fever for at least 72 hours.

Treat sustained ICP above 22 mmHg (BTF 4th ed., Level IIB); target CPP 60-70 mmHg, with the optimal value within that range depending on the patient's autoregulatory status. Avoid aggressively pushing CPP above 70 with fluids/pressors due to ARDS risk.

Alteplase 0.9 mg/kg (max 90 mg; 10% bolus, remainder over 60 minutes) or tenecteplase 0.25 mg/kg as a single IV bolus (max 25 mg), within 4.5 hours of onset for eligible disabling deficits - the 2026 guideline lists both as Class 1 options.

Lower BP below 185/110 mmHg before IVT and keep it below 180/105 mmHg for at least 24 hours after. After IVT, targeting SBP below 140 gives no benefit (2026 AHA/ASA, COR 3: No Benefit); after successful thrombectomy recanalization, SBP below 140 for 72 hours is harmful (COR 3: Harm).

Anterior ICA/M1 occlusion with NIHSS ≥6 and prestroke mRS 0-1: EVT within 6 hours for ASPECTS 3-10, and at 6-24 hours for ASPECTS ≥6 (or 3-5 if age <80 without mass effect) (2026 AHA/ASA, COR 1). Basilar occlusion: EVT within 24 hours if NIHSS ≥10 and PC-ASPECTS ≥6.

For large MCA-territory infarction with progressive midline shift or herniation despite maximal medical therapy, typically within 48 hours of onset in patients under about 60 years - pooled trial data show reduced mortality, though survivors often have significant residual disability.

In mild-to-moderate ICH presenting with SBP 150-220 mmHg, lowering to a target of 140 mmHg and keeping it within 130-150 mmHg may be reasonable (2022 AHA/ASA, COR 2b). Lowering SBP below 130 mmHg is potentially harmful (COR 3: Harm). Start within 2 hours of onset and reach target within 1 hour.

Immediately, with or without an EVD, if the patient is deteriorating neurologically, has brainstem compression or hydrocephalus from ventricular obstruction, or the hematoma volume is at least 15 mL - in preference to medical management alone to reduce mortality (2022 AHA/ASA ICH guideline, COR 1).

Hunt-Hess and the WFNS scale grade clinical severity from GCS/exam findings; the modified Fisher scale grades hemorrhage burden on CT to predict delayed cerebral ischemia risk. Higher grades on either scale type correlate with worse functional outcome.

Enteral nimodipine 60 mg every 4 hours for 21 days is given to all aneurysmal SAH patients regardless of vasospasm status (2023 AHA/ASA). Delayed cerebral ischemia risk peaks between days 4 and 14 after the bleed - the window for closest monitoring.

Epidural: usually arterial (middle meningeal artery) after temporal skull fracture, biconvex/lentiform, does not cross suture lines, tends to expand faster. Subdural: venous (bridging veins), crescent-shaped, can cross suture lines - epidural typically needs more urgent evacuation.

The 2024 AO Spine/Praxis guideline suggests augmenting MAP to at least 75-80 mmHg but not above 90-95 mmHg for 3-7 days (weak recommendation), replacing the older AANS/CNS target of 85-90 mmHg for 7 days. Avoid hypotension (SBP below 90 mmHg).

A single continuous convulsive seizure lasting 5 minutes or longer, OR two or more seizures without full return to baseline consciousness between them - treatment begins at this 5-minute mark rather than waiting for the older 30-minute definition.

IM midazolam 10 mg (over 40 kg) as a single dose, IV lorazepam 0.1 mg/kg (max 4 mg, may repeat once), or IV diazepam 0.15-0.2 mg/kg (max 10 mg, may repeat once) - AES 2016 guideline, all three considered equivalent first-line options.

The '20/30/40 rule': vital capacity under 20 mL/kg, maximum inspiratory pressure less negative than -30 cmH2O, or maximum expiratory pressure under 40 cmH2O - any one predicts high risk of needing mechanical ventilation and should prompt ICU-level monitoring or elective intubation.

Evidence does not support routine long-term prophylaxis in patients without a prior seizure history; when used at all, it is typically limited to a brief perioperative course. Antiseizure drugs are indicated for patients who actually have a seizure, not as blanket prophylaxis.

A CSF leak, with possible associated pneumocephalus. Clear rhinorrhea or otorrhea after skull-base or transsphenoidal surgery raises meningitis risk and often needs urgent evaluation; beta-2 transferrin testing of the fluid confirms CSF when the diagnosis is uncertain.

Ventriculitis/CSF infection, with risk rising after roughly 5-7 days of catheterization. Risk is reduced with sterile insertion technique, antibiotic-impregnated catheters, and minimizing unnecessary manipulation - not by routine scheduled catheter exchange, which does not reliably lower infection rates.

If clinicians predict a poor outcome too early and withdraw life-sustaining therapy, the prediction becomes self-confirming. Avoid early limitation of care based on a single finding or severity score; after cardiac arrest, multimodal prognostication (exam, EEG, SSEP, biomarkers, imaging) is deferred to at least 72 hours after ROSC or normothermia (2025 AHA).

In DBD, death is declared by neurologic criteria while circulation and organ support continue until procurement. In DCD, death is declared after circulatory arrest following withdrawal of life-sustaining therapy - organ ischemia time and eligible organs differ between the two pathways.