Hyperacute stroke care, the first hours

A 0 requires both questions answered correctly; an intubated patient cannot give the answers, and the scale does not accept written or gestured replies here.

Marking the item untestable is a common shortcut, but the NIHSS gives a defined score for intubation; UN is used only on a few items such as limb motor after amputation or joint fusion.

The NIHSS rules score item 1b as 1 when a patient cannot speak because of intubation or orotracheal trauma, even if the patient is alert and following commands.

A 2 is reserved for aphasic or stuporous patients who cannot understand the questions; an alert, command-following patient does not meet that description.

Ptosis with a dilated pupil points to a third-nerve palsy; loss of sympathetic tone makes the pupil smaller, not larger.

A carotid dissection stretches the sympathetic fibers on the wall of the internal carotid, so ptosis and a small pupil appear on the same side; facial sweating is usually spared because the sweat fibers to the face travel with the external carotid.

These are the right signs on the wrong side; the sympathetic fibers are injured at the dissected carotid, so the signs are ipsilateral, not contralateral.

Lid retraction and a large pupil are signs of sympathetic overactivity, the opposite of the loss of sympathetic tone in Horner syndrome.

Malignant edema shows as swelling with mass effect and midline shift a day or more after a large infarct, not as tissue loss.

The penumbra is usually invisible on noncontrast CT and is found with perfusion imaging; old white matter change is not penumbra.

Early ischemia blurs the gray-white boundary in the cortex or basal ganglia; it does not cause encephalomalacia, which takes weeks to form.

Patchy periventricular white matter hypodensity is chronic small-vessel disease, and encephalomalacia is softened, CSF-like tissue left by an old infarct; neither is the new lesion.

Entering the dose in mg/h as the rate in mL/h is a classic pump error; at 0.2 mg/mL it would deliver only 1.5 mg/h.

At 0.2 mg/mL, 150 mL/h delivers 30 mg/h, four times the order and twice the usual 15 mg/h maximum; a check of mL/h × mg/mL catches it.

This rate fits the other premix strength, 20 mg in 200 mL (0.1 mg/mL); reading the wrong bag concentration doubles the dose.

The bag holds 40 mg in 200 mL, or 0.2 mg/mL, so 7.5 mg/h divided by 0.2 mg/mL gives 37.5 mL/h.

Vitamin K by slow IV infusion restarts synthesis of factors II, VII, IX and X within hours and keeps the INR down after the short-acting PCC wears off; slow infusion limits the rare anaphylactoid reaction.

Subcutaneous absorption is erratic and slow, so this route is no longer recommended for urgent warfarin reversal.

An intramuscular injection risks a hematoma in an anticoagulated patient, and 1 mg is a dose for mild INR elevation, not for a life-threatening bleed.

Oral vitamin K is used for an elevated INR without bleeding; in an intracranial bleed its slower, less reliable absorption risks a rebound INR when the PCC effect fades.

Hemicraniectomy decompresses a swollen supratentorial (MCA) infarct; it does nothing for pressure in the posterior fossa.

Steroids do not reduce the cytotoxic edema of an infarct and are not recommended for post-stroke swelling.

A swelling cerebellar infarct that compresses the brainstem and blocks CSF flow is treated by opening the posterior fossa; it is lifesaving and survivors often recover well.

With a posterior fossa mass and obstructive hydrocephalus, an LP can cause downward herniation; CSF is drained from above with a ventricular drain if needed.

Blooming on gradient-echo or SWI shows blood products or microbleeds, not the ischemic core.

Diffusion-weighted imaging shows the tissue where cell swelling has already set in, which approximates the irreversible core used in late-window thrombectomy selection.

A delayed Tmax marks the whole underperfused area, mostly penumbra; the mismatch between it and the core is what selects late-window patients.

FLAIR change appears hours after onset and helps estimate timing in wake-up strokes; it is not the measure of core volume.

ASPECTS is scored on the noncontrast CT, and core volume comes from perfusion imaging; neither needs the neck.

The mismatch ratio comes from CT perfusion or MRI, not from angiography of the neck vessels.

Hemorrhage is excluded by the noncontrast head CT, and the lytic should not wait for CTA of any region.

Imaging from the aortic arch to the vertex shows a cervical carotid occlusion or dissection behind the intracranial clot and the route the catheter must take, which changes the thrombectomy plan.

No partial-dose strategy exists; a reduced dose gives less benefit with the same bleeding risk.

The patient is eligible and 2 hours from last known well, and every minute of delay costs brain; under the stroke protocol the emergency physician can order thrombolysis without waiting for the neurologist.

The first CT already excluded hemorrhage 25 minutes ago; repeating it adds delay without adding information.

Waiting for a consultant who cannot be reached lets the patient drift toward the end of the window; the protocol exists so treatment does not depend on one person.

Oxygen and watching do not open a closing airway; relying on them delays the definitive airway until intubation becomes impossible.

A blind nasal tube through swollen tissue often fails, and in a patient who just received a lytic it risks severe nasal bleeding.

Stridor and floor-of-mouth swelling mean the airway is closing despite drug treatment; awake fiberoptic intubation secures it while the patient keeps breathing, and a surgical airway is the backup.

The antihistamine and steroid have already failed, and an hour is too long to wait with stridor; lytic angioedema is partly bradykinin-driven and may not respond.

Iodinated contrast from the procedure can pool in injured tissue and look like blood; in a patient who is improving, follow-up CT or dual-energy CT tells staining, which fades, from a real bleed.

A new infarct is dark (hypodense) on CT and does not show this early; a bright area is blood or contrast.

Calling it a definite bleed right after thrombectomy ignores contrast staining, and giving reversal agents to an improving patient adds risk without a confirmed hemorrhage.

The density is new compared with the earlier scan, so it cannot be old calcification.

Door-to-CT, at 35 to 42 minutes, is the longest step, roughly double the next one; prenotification lets the team meet the ambulance and go straight to the scanner.

A second interventional team speaks to thrombectomy access, not to the lytic delay in these cases, and none of the measured intervals involves it.

Adding a step before the decision lengthens the CT-to-decision interval instead of fixing the door-to-CT delay.

Better time-stamps make the data more accurate, but measuring a delay does not shorten it.

Securing an incidental small aneurysm first would take the patient out of the treatment window; the bleeding risk of the aneurysm is low and does not justify the delay.

Full-dose heparin does not treat acute ischemic stroke and adds bleeding risk without recanalizing the artery.

A small (under 10 mm) unruptured, unsecured aneurysm found on CTA does not exclude an otherwise eligible patient, and BP is already within the lytic range.

A reduced dose has no evidence base; it lowers the benefit while leaving the bleeding risk in place.

A faster coagulation test still keeps a test that this group of patients does not need; it shortens the wait instead of removing it.

Adding a consult before treatment makes the delay longer and more variable instead of removing it.

Splitting the bolus from the infusion breaks the dosing schedule and still makes the full dose wait for an unneeded result.

Glucose is the only lab required before a lytic; when nothing suggests anticoagulant use or a bleeding disorder, waiting for PT/INR and platelets only adds door-to-needle time.

Waiting half an hour leaves the patient above the post-lytic limit, which raises the risk of symptomatic hemorrhage.

During and after a lytic the BP must stay below 180/105 mm Hg; a reading above it is treated at once with an IV agent and rechecked soon after, while the infusion continues.

An oral beta-blocker acts too slowly and unpredictably to bring BP under the limit quickly; IV titratable agents are used.

The infusion is stopped for neurologic decline, severe headache, angioedema or bleeding; a high BP with a stable exam is treated, not a reason to stop.

Hunt and Hess grade 3 is drowsiness or confusion with at most a mild focal deficit, which is exactly this picture.

Grade 2 is a moderate to severe headache with neck stiffness and no deficit other than a cranial nerve palsy; drowsiness moves the patient higher.

Grade 4 is stupor with moderate to severe hemiparesis; this patient is drowsy but rousable with only mild weakness.

Grade 1 is no symptoms or mild headache with slight neck stiffness; a confused, drowsy patient is beyond it.

Giving the oral product IV, even slowly, is the exact error behind the boxed warning; it can cause profound hypotension and cardiac arrest.

Diluting the oral liquid does not make it safe for a vein; the US has no IV nimodipine product, and any parenteral route is prohibited.

A central line gives the drug even faster access to the heart; this is the same parenteral error that led to the warning.

Nimodipine carries a boxed warning against parenteral use: liquid drawn from capsules or an oral solution given IV has caused cardiac arrest and death, so it goes only by mouth or enteral tube in an oral syringe.

The TNKase label for stroke doses by weight band, and every patient who weighs 90 kg or more gets the 25 mg maximum as one IV bolus over about 5 seconds.

Multiplying 0.25 mg/kg by 110 kg ignores the ceiling; the stroke dose stops rising at 25 mg from 90 kg up.

50 mg is the label dose for STEMI in patients 90 kg or more, twice the stroke dose; mixing up the two indications overdoses the stroke patient.

A 10% bolus with the rest infused over an hour at 0.9 mg/kg, capped at 90 mg, is the alteplase regimen; tenecteplase needs no infusion.