Free SCRN Exam Flashcards

The last time the patient was confirmed at neurologic baseline, NOT the time symptoms were discovered. If a patient was normal at 2230 and woke aphasic at 0700, LKW is 2230. LKW drives thrombolytic and thrombectomy eligibility decisions.

Activate the stroke pathway as soon as a new focal deficit is suspected—not after imaging confirms ischemic stroke. Aspirin, oral intake, and routine admission tasks must not delay hemorrhage exclusion or reperfusion screening.

Balance, Eyes, Face, Arm, Speech, Time. A normal face-arm-speech check does not make a patient safe: posterior circulation strokes can present with isolated imbalance, diplopia, or dysphagia and still be time-critical.

An immediate triage priority because severe hypoglycemia can mimic focal weakness, speech change, or altered mental status. Treat abnormal glucose and reassess the deficit before the team commits to thrombolytic therapy.

Nonvascular processes that resemble stroke: hypoglycemia, postictal (Todd) paralysis, complex migraine, infection, intoxication, and functional symptoms. Assess them rapidly without delaying stroke activation—treat as stroke until proven otherwise.

A standardized scale that quantifies stroke severity and trends neurologic change. A low total can still miss disabling aphasia, visual loss, neglect, or posterior circulation danger, so bedside surveillance must supplement the number.

A meaningful neuro assessment compares the current exam to the documented baseline, not only to textbook normal. Worsening relative to that patient's baseline—even if still 'abnormal'—is the trend that triggers escalation.

Widening pulse pressure (rising systolic, falling diastolic), bradycardia, and irregular respirations. A late, ominous sign of rising intracranial pressure—escalate immediately and prepare for urgent imaging and possible neurosurgical intervention.

New decreased consciousness, worsening NIHSS elements, severe headache, vomiting, seizure, pupillary change, or new focal deficit. Stop routine tasks, reassess ABCs/glucose/vitals, notify the stroke team, and prepare for imaging.

Aphasia is impaired language processing (comprehension or expression), usually from dominant-hemisphere injury. Dysarthria is impaired speech motor output with intact language. Confusing them leads to inaccurate assessment and unsafe education.

Contralateral face and arm weakness greater than leg, gaze deviation, and sensory loss. Dominant hemisphere adds aphasia; nondominant adds neglect and anosognosia. Protect the ignored side and anticipate unsafe transfers.

Contralateral leg weakness greater than arm, abulia (impaired initiation), frontal behavior change, and urinary symptoms. Do not mistake low initiation for refusal or noncompliance; assess transfer and toileting safety.

Homonymous visual field loss, cortical blindness, thalamic sensory pain, and memory changes. Screen for visual neglect, reading difficulty, and unsafe ambulation related to the field cut.

Dizziness, diplopia, dysarthria, dysphagia, ataxia, or depressed consciousness. Easily under-triaged because symptoms seem less dramatic than hemiplegia. Prioritize airway, swallow risk, and rapid escalation for decline.

A neurologic emergency that can progress to quadriplegia, coma, or locked-in syndrome. Subtle early symptoms (dysarthria, diplopia, decreased arousal) can precede catastrophic decline—treat new posterior signs as escalation findings.

Small deep-vessel stroke producing pure motor or sensorimotor deficits WITHOUT cortical signs (no aphasia, neglect, or visual field cut). Trend subtle changes; do not assume a small-appearing stroke is automatically low risk.

The core is irreversibly injured tissue; the penumbra is impaired but potentially salvageable if circulation is restored in time. Saving the penumbra is the rationale for time-critical reperfusion therapy.

Transient focal ischemia whose symptoms resolve without persistent deficit. It is NOT reassuring—it signals unstable cerebrovascular risk requiring urgent evaluation and prompt secondary prevention, not discharge with reassurance alone.

Fast and widely available; its primary job is to exclude intracranial hemorrhage before thrombolytic therapy. A normal early CT does NOT rule out disabling ischemia—keep the stroke pathway moving rather than reassuring the patient.

CTA from the aortic arch through the head identifies large-vessel occlusion and vascular anatomy, supporting thrombectomy routing or transfer. Nursing prep: IV access, contrast allergy screen, and rapid transport.

Identifies infarct core versus salvageable tissue for selected patients with wake-up stroke, unknown onset, or later presentation—expanding reperfusion options beyond simple time windows.

Target: Stroke / Get With The Guidelines tracks door-to-needle within 60 minutes for treated patients and brain imaging within ~20-25 minutes. The tested behavior is EMS prenotification, single-call activation, and direct-to-CT transport.

Current acute ischemic stroke guidance supports IV alteplase or tenecteplase for eligible patients within the 4.5-hour window, with advanced-imaging selection for some later or unknown-onset cases. Local protocol sets the agent and dosing.

Confirm last known well, dosing weight, glucose, baseline NIHSS, vitals, anticoagulant use and last dose, allergies, recent surgery/trauma, and IV access—run these in parallel with imaging, never sequentially after it.

Hemorrhage on imaging, active internal bleeding, recent intracranial/spinal surgery or serious head trauma, severe uncontrolled hypertension, very low platelets, or anticoagulant-related coagulopathy. The nurse escalates these; the provider decides.

Severe hypertension must be lowered to the protocol threshold before IV thrombolysis can proceed, because elevated pressure increases hemorrhage risk. After treatment, follow ordered parameters and report excursions promptly.

Severe headache, vomiting, acute hypertension, worsening neurologic status, or tongue/lip swelling (angioedema). Stop the infusion if running, notify urgently, and prepare for airway management and emergent imaging.

Gaze deviation, dense hemiparesis, global aphasia, severe neglect, depressed consciousness, or a very high NIHSS. A modest NIHSS does not remove concern in posterior or aphasic strokes—activate the team and keep imaging moving.

Endovascular clot removal for selected large-vessel-occlusion patients. Current guidance broadens eligibility, so later arrival, wake-up stroke, or early ischemic change does not automatically end the thrombectomy conversation.

Hospitals without thrombectomy capability must prioritize rapid vascular imaging, telestroke or specialist input, and a fast door-in-door-out transfer for eligible LVO patients—bedside delays cost salvageable tissue.

Neurologic trending, ordered blood pressure management, arterial access-site checks, distal pulse assessment, and bleeding surveillance. Escalate immediately for neurologic decline or access-site hematoma.

Avoid aggressive normalization because cerebral perfusion may be pressure-dependent. Do not chase a normal outpatient BP in the first hours unless above the protocol threshold or another emergency exists.

Avoid both hyperglycemia and hypoglycemia; many inpatient protocols target roughly 140-180 mg/dL. Guidance cautions against intensive control to 80-130 mg/dL because it adds severe hypoglycemia risk without improving outcome.

Elevated temperature can worsen neurologic injury. Report and treat fever per protocol with normothermia measures and evaluate for infection or other causes—do not treat post-stroke fever as benign.

All stroke patients need swallowing safety assessed before any oral food, fluids, or medications because silent aspiration is common. Keep NPO until a swallow screen clears the patient.

Immobile stroke patients are at venous thromboembolism risk. Eligible patients should receive prophylaxis or have a documented reason for none—a tracked Joint Commission STK quality measure.

Airway, neurologic trend, smooth sustained BP control to limit hematoma expansion, rapid anticoagulant reversal by drug type, hematoma-expansion surveillance, and neurosurgical readiness.

Reversal commonly involves vitamin K plus 4-factor prothrombin complex concentrate. Dabigatran and factor Xa inhibitors have specific reversal strategies. The nurse escalates immediately rather than independently selecting the agent.

Thunderclap (sudden, worst-ever) headache, meningeal signs, vomiting, photophobia, syncope, or collapse—even when focal weakness is limited. Suspect aneurysmal SAH and escalate urgently.

Enteral nimodipine is given when ordered to improve outcomes related to delayed cerebral ischemia. Monitor for hypotension after doses and communicate if a dose is held or not tolerated.

Before the aneurysm is secured, prevent rebleeding by controlling pain, nausea, agitation, and severe blood pressure elevations while avoiding hypotension. Sudden re-deterioration suggests rebleeding—escalate at once.

Cerebellar infarction or hemorrhage can worsen from edema and obstructive hydrocephalus even when early limb strength is preserved. Trend headache, vomiting, and arousal; prevent falls.

Formal interdisciplinary rehab assessment begins in the hospital once the patient is medically stable, but high-dose very early mobilization within the first 24 hours of onset can be unsafe—progress activity to neurologic and hemodynamic stability.

The nervous system's experience-dependent ability to reorganize after injury. Nurses support it by protecting sleep, nutrition, oxygenation, glucose, mood, skin, and participation in safe task-specific practice.

Aspiration, falls, pressure injury, venous thromboembolism, shoulder injury, delirium, depression, and medication-related bleeding. SCRN items often link a syndrome to its downstream risk (neglect to falls, brainstem to aspiration).

The plan depends on cause: non-cardioembolic, cardioembolic, large-artery, small-vessel, cryptogenic, or hemorrhagic stroke do not use the same regimen. Ask what caused the stroke before choosing therapy.

AF-related (cardioembolic) stroke is usually prevented with anticoagulation, NOT antiplatelet monotherapy. Discharge teaching must reinforce anticoagulant purpose, adherence, bleeding precautions, and follow-up.

DAPT is not a long-term default. It is reserved for selected high-risk scenarios (e.g., early minor stroke or high-risk TIA) as a prescribed short course—teach patients not to continue it indefinitely on their own.

Asking the patient or caregiver to explain or demonstrate the plan in their own words. It tests how clearly the team taught, not the patient's intelligence, and outperforms asking 'Do you understand?'—essential with aphasia or low health literacy.

Core discharge education elements: activate EMS for symptoms, follow-up after discharge, medications prescribed at discharge, risk factors for stroke, and warning signs/symptoms—adapted to the patient's deficits and health literacy.