6.1 Stroke, TBI & Space-Occupying Lesions

Stroke, TBI & Space-Occupying Lesions

Neurologic emergencies in progressive care demand rapid recognition because delays in treatment translate directly into lost brain tissue. Progressive care nurses must be fluent in stroke classification, intracranial pressure (ICP) management, and the herniation syndromes produced by expanding intracranial lesions.

Ischemic vs. Hemorrhagic Stroke

Stroke is divided into two categories that require opposite initial management, which is why a non-contrast head CT is mandatory before any thrombolytic is given:

• Ischemic stroke (about 87% of strokes) results from thrombotic or embolic occlusion of a cerebral vessel, cutting off blood flow to brain tissue.
• Hemorrhagic stroke (about 13%) results from vessel rupture — intracerebral or subarachnoid — and administering a thrombolytic to a hemorrhagic stroke patient would be catastrophic.

The NIH Stroke Scale (NIHSS) quantifies deficit severity (0 = no deficit; higher scores = more severe deficit) and is repeated serially to detect improvement or deterioration. Common findings include facial droop, unilateral weakness, dysarthria or aphasia, and visual field cuts.

Time Is Brain: Thrombolytic and Thrombectomy Windows

For eligible ischemic stroke patients, IV alteplase (tPA) should be given within 4.5 hours of last known well, after hemorrhage is excluded by CT and contraindications (recent surgery, active bleeding, therapeutic anticoagulation, uncontrolled blood pressure above 185/110) are ruled out. Blood pressure must be controlled before and after thrombolysis to reduce hemorrhagic-conversion risk. For patients with a large-vessel occlusion, mechanical thrombectomy can extend the treatment window up to 24 hours in carefully selected patients using perfusion imaging, even when they fall outside the tPA window.

Nursing priorities after thrombolysis include neurologic checks every 15 minutes for the first two hours (watching for any decline suggesting hemorrhagic conversion), strict blood pressure limits, avoiding invasive lines or NG tubes for 24 hours, and holding antiplatelet or anticoagulant therapy until repeat imaging confirms safety.

Intracranial Pressure and the Cushing Triad

Normal ICP is roughly 5–15 mmHg; sustained ICP greater than 20–22 mmHg is treated aggressively per Brain Trauma Foundation guidelines because it compromises cerebral perfusion pressure (CPP = MAP − ICP), with a target CPP generally kept 60–70 mmHg. Early signs of rising ICP are subtle — decreasing level of consciousness is the single earliest and most reliable indicator, along with headache, vomiting, and pupillary change. The Cushing triad — hypertension with a widening pulse pressure, bradycardia, and irregular respirations — is a late and ominous sign reflecting brainstem compression, not an early warning.

Management includes head-of-bed elevation to 30 degrees with neutral head and neck alignment, avoiding hip flexion, treating fever and pain, osmotic therapy (mannitol or hypertonic saline), sedation, and CSF drainage via an external ventricular drain (EVD) when placed. EVD nursing requires leveling the transducer at the tragus, maintaining a closed sterile system, and monitoring drainage volume and character alongside continuous ICP waveforms.

Space-Occupying Lesions and Herniation

Traumatic brain injury (TBI), brain tumors, subdural hematomas, and abscesses all raise ICP by adding mass within the fixed cranial vault. TBI severity is graded using the Glasgow Coma Scale (GCS), scored across three components:

Total GCS ranges 3–15: mild TBI is 13–15, moderate is 9–12, and severe is 8 or below, which often prompts intubation for airway protection. Acute subdural hematomas develop rapidly from venous bleeding after trauma, while chronic subdurals accumulate slowly, particularly in older or anticoagulated patients, and may present with vague cognitive change weeks after a seemingly minor fall.

As mass effect increases, brain tissue shifts and herniates. A dilated, sluggish, or fixed ("blown") pupil ipsilateral to the lesion signals uncal herniation compressing cranial nerve III — a neurosurgical emergency. Decorticate posturing (arms flexed toward the core) indicates a less severe lesion level than decerebrate posturing (arms extended and rigid), which reflects brainstem involvement. Continuous EEG monitoring may be used in patients with unexplained decreased responsiveness to detect nonconvulsive seizures contributing to the picture. Any acute neurologic decline in a patient with a known space-occupying lesion warrants immediate reassessment and often an urgent repeat CT, since surgical decompression may be time-critical.

Nursing Considerations Across the Continuum

Several cross-cutting issues apply to nearly every patient in this section. Fever worsens secondary brain injury by increasing cerebral metabolic demand, so aggressive normothermia (antipyretics, cooling devices) is standard after stroke, TBI, and any acute brain insult. Seizure prophylaxis is often used for the first week after moderate-to-severe TBI or intracranial hemorrhage, since early post-injury seizures are common and increase metabolic demand on already-injured tissue. Sodium disturbances are also frequent in neurologic injury: SIADH causes hyponatremia through water retention and is managed with fluid restriction, while cerebral salt wasting causes hyponatremia through renal sodium loss and is managed with sodium and volume replacement — distinguishing the two matters because the treatments are opposite. Finally, every immobile neurologic patient needs venous thromboembolism prophylaxis (mechanical initially, pharmacologic once bleeding risk allows) and a structured plan for early rehabilitation referral, since functional outcomes after stroke and TBI depend heavily on how quickly therapy begins.