| Personnel and environmental configuration |
| Multidisciplinary collaboration | 1. For patients with aSAH, care should be provided in a dedicated neurocritical care unit by a multidisciplinary team13 | 1 | A | Direct | Suspected aSAH triage (<6 h from onset) | - |
| Stroke unit establishment | 2. Acute stroke unit care reduces both death and dependency for patients with ICH in comparison with care on a general ward23 | 1 | A | Indirect | Confirmed aSAH critical monitoring (days 3-14) | - |
| 3. Patients with intracerebral hemorrhage should be directly transferred to a hyperacute specialized stroke unit for consciousness tracking; any acute neurological deterioration dictates urgent re-imaging21,23 | 5 | B | Indirect | Hunt-Hess II-IV patients requiring serial GCS tracking | Impending brainstem herniation requiring immediate surgery |
| BP control targets |
| Principles of BP control | 4. Maintain systolic blood pressure (SBP) strictly between 120–160 mmHg and ensure mean arterial pressure (MAP) stays above 90 mmHg in aSAH cohorts to mitigate re-rupture secondary to hypoperfusion10,16,19–21,25 | 5 | A | Direct | Before aneurysm securing interval of ruptured unsecured aneurysm | Patients with severe intracranial hypertension (ICP >25 mmHg) or compromised CPP require individualized blood pressure targets to avoid CPP reduction resulting from excessive blood pressure lowering |
| 5. Following surgical securing of the aneurysm, sustain MAP within 80–100 mmHg provided the patient presents no signs of intracranial hypertension or cerebral vasospasm17 | 1 | A | Direct | After aneurysm securing phase (clipped/coiled) without vasospasm | In patients with symptomatic cerebral vasospasm or DCI, induced hypertension may be required; therefore, these blood pressure targets should not be applied rigidly |
| History of hypertension | 6. For patients presenting with a history of chronic hypertension or presenting clear radiological features of intracranial hypertension, titrate SBP and MAP toward their upper safety boundaries (160 mmHg and 100 mmHg, respectively)16 | 3 | B | Direct | aSAH with chronic poorly controlled hypertension baseline | Micro-aneurysm morphology showing active acute rebleeding signs |
| No history of hypertension | 7. For individuals lacking a hypertensive history or signs of elevated intracranial pressure, target the lower operational boundaries (SBP near 120 mmHg; MAP near 80 mmHg)16 | 5 | B | Direct | Young, previously normotensive patients (Hunt-Hess I-II) | New focal deficits indicating active cerebral hypoperfusion. |
| BP monitoring |
| Monitoring method | 8. Utilize invasive continuous intra-arterial tracking or standardized non-invasive modalities for precise post-operative SBP surveillance10,11 | 2 | A | Direct | Beat-to-beat tracking during rapid continuous IV titration | Severe peripheral arterial disease preventing arterial cannulation |
| Monitoring frequency | 9. Record blood pressure immediately upon emergency presentation, maintaining a 15-min tracking frequency until therapeutic targets achieve documented stability within the initial 24 h18 | 5 | A | Indirect | First 24 h of admission or active infusion adjustments | Stable maintenance phases (>48 h post-op) on fixed doses |
| Management principles | 10. For cases presenting acute intraparenchymal bleeding, initiate antihypertensive titration within 2 h of symptom onset; ensure the overall SBP reduction does not drop beyond 90 mmHg from baseline parameters12,19 | 1 | A | Indirect | Stress-induced SBP spikes (>180 mmHg) post-rupture | Precipitous, abrupt iatrogenic SBP reductions inducing infarction |
| 11. Implement systematic and gradual reduction of elevated SBP thresholds in patients presenting with un-occluded or unsecured aneurysms9,12 | 1 | A | Direct | Controlled, step-wise SBP down-titration pre-operatively | Induced profound iatrogenic systemic hypotension (SBP <100 mmHg) |
| 12. Enforce strict vigilance to prevent post-operative systemic hypotension following the repair of ruptured intracranial aneurysms10,11 | 1 | A | Direct | Post-operative daily maintenance during vasospasm window | - |
| 13. Prioritize short-acting, highly titratable intravenous agents (e.g., nicardipine or labetalol) when active BP lowering is required; routinely avoid potent cerebral vasodilators such as nitroprusside or nitroglycerin to prevent hemodynamic volatility9,12,18,20 | 1 | A | Direct | Acute neurocritical settings requiring second-by-second SBP control | Routine use of vasodilators that may increase intracranial pressure, such as sodium nitroprusside, is not recommended. In selected circumstances, potential benefits should be carefully weighed against risks with close monitoring |
| 14. In patients with acute aSAH and unsecured aneurysms, frequent blood pressure monitoring and tailored BP control leveraging short-acting medications are highly recommended to strictly avoid severe hypotension, extreme hypertension, and pathological BP variability prior to definitive vascular securing13 | 5 | A | Direct | Hyperacute before aneurysm securing window (<24 h from symptom onset) | Intermittent manual IV boluses without continuous physiological tracking |
| 15. In patients with acute intracerebral hemorrhage displaying severe hypertensive spikes (SBP >200 mmHg or MAP >150 mmHg), contemplate rapid, intensive blood pressure reduction supported by 5-min tracking intervals24 | 2 | B | Indirect | Malignant hypertensive crisis (SBP >200 mmHg) before aneurysm securing | Terminal structural failure (bilateral fixed mydriasis) |
| 16. For intraparenchymal bleeding cases with SBP >180 mmHg or MAP >130 mmHg accompanied by clear signs of intracranial hypertension, continuously track ICP and adjust intravenous titrations to safeguard a cerebral perfusion pressure (CPP) window of 61–80 mmHg24 | 1 | A | Indirect | Comatose high-grade aSAH with functional invasive ICP monitors | Aggressive empirical BP lowerings without real-time CPP tracking |
| 17. For intraparenchymal bleeding cases with SBP >180 mmHg or MAP >130 mmHg but without elevated ICP clinical indicators, lower the blood pressure moderately and mandate formal clinical re-evaluations every 15 min24 | 3 | B | Indirect | Alert patients with stable baseline intracranial compliance | Sudden explosive headache or projectile vomiting (suspected micro-rupture) |
| 18. If patients requiring continuous blood pressure maintenance possess intact, functional swallowing mechanisms, safely resume their established pre-admission oral antihypertensive regimens19 | 1 | A | Indirect | Post-op plateau phase where patient tolerates oral intake | Persistent depressed consciousness levels or severe neuro-agitation |
| 19. In the presence of acute dysphagia or altered consciousness levels, temporarily withhold prior oral medications and substitute with intravenous titrations until swallowing function stabilizes or a nasogastric pathway is secured19 | 1 | A | Indirect | Patients with lower cranial nerve palsies or bulbar paralysis | Oral administration without screening (absolute fatal aspiration risk) |
| Non-pharmacological interventions | 20. Minimize external environmental triggers and defer non-urgent invasive bedside nursing tasks to safeguard patient calmness and prevent paroxysmal rebleeding episodes10 | 1 | A | Direct | Standard non-pharmacological neuro-protection routine in single rooms | - |
| 21. Enforce strict bed rest regimes, execute systematic bowel regularity protocols to avoid straining, and maintain accurate hourly monitoring of systemic fluid inputs and outputs9,10,12,20 | 1 | A | Direct | Pre-operative immobilization to minimize transmural pressure spikes | Bowel management interventions that may provoke a Valsalva maneuver or cause significant blood pressure fluctuations should be avoided |
| 22. Manage severe headache presentations or psychomotor agitation with minimal effective dosing of analgesics and sedatives; implement early weaning protocols as clinical tolerance permits9,11 | 1 | A | Direct | Thunderclap headache/agitation driving sympathetic hypertensive loops | Excessive sedation that interferes with neurological assessment should be avoided; daily sedation interruption or awakening trials should be considered when clinically appropriate |
| Complication prevention |
| DCI | 23. Utilize specialized neurovascular imaging techniques (e.g., CTA or CTP) to detect subclinical vasospasm and predict the onset of delayed cerebral ischemia (DCI) when physical examinations are restricted10,13,20 | 1 | A | Direct | High-grade, sedated aSAH where serial clinical exam is impossible | Fully alert, neurologically stable low-grade patients |
| 24. For high-grade aSAH cohorts, consider advanced invasive neuromonitoring parameters, including brain tissue oxygen tension and localized microdialysis (lactate/pyruvate and glutamate ratios), to predict DCI trends13 | 2 | B | Direct | Severe, high-grade thick clot patients (modified Fisher 4) post-op | Community centers lacking multimodality sensor calibration tools |
| 25. Standardize the application of validated neurological tracking tools (such as GCS and NIHSS scores) to perform serial assessments for DCI and secondary neurovascular declines10,21,25 | 1 | A | Direct | Shift-to-shift handovers and quantitative serial tracking for DCI | - |
| Cerebral vasospasm | 26. Maintain normovolemia to prevent DCI; routine prophylactic hypervolemia is not recommended14 | 2 | A | Direct | Asymptomatic postoperative phase within the DCI risk window | Patients with symptomatic cerebral vasospasm require individualized volume and blood pressure management based on cerebral perfusion status |
| 27. Schedule transcranial Doppler (TCD) scans daily or every other day to perform regular screening for vasospasm trajectories in aSAH patients14 | 1 | A | Direct | Bedside non-invasive velocity screening during peak vasospasm window | - |
| 28. Administer standard oral nimodipine regimens for vasospasm prophylaxis; implement continuous intravenous nimodipine infusions as an authorized alternative only if oral/enteral ingestion pathways are compromised10–12,14,15,20–23,25 | 1 | A | Direct | Routine pharmacological neuro-protection for all confirmed aSAH cases | In patients with refractory systemic hypotension (SBP <90 mmHg), nimodipine dose adjustment, temporary discontinuation, or alternative treatment strategies should be considered |
| 29. Dual antiplatelet therapeutic approaches may be considered to lower the overall incidence of clinical vasospasm and secondary DCI events10,19 | 1 | B | Direct | Subpopulation undergoing endovascular coiling with stent placement | Early phases of open clipping, unsecured aneurysms, or coagulopathy |
| Volume management |
| 30. Avoid the routine preoperative implementation of hypervolemia, hemodilution, and hypertensive therapy (traditional 3H protocols); restrict these interventions strictly to SAH individuals with documented hypovolemic states19,21 | 1 | A | Direct | Fluid profiling of neurologically intact, normovolemic perioperative patients | Prophylactic traditional 3H therapy in asymptomatic cohort |
| 31. Determine fluid status by combining clinical volume assessments with hemodynamic monitoring parameters14 | 2 | A | Direct | Dynamic fluid balance titration during intensive neurocritical monitoring | Empirical fluid bolus ordering without baseline hemodynamic checks |
| Follow-up | | | | | | |
| 32. Arrange the initial post-operative neuroimaging follow-up window at 3–6 months, followed by serial surveillance at years 1, 2, 3, and 5, transitioning subsequently to a 3-to-5-year maintenance interval19 | 1 | A | Direct | Outpatient surveillance tracking coil compaction or recurrence | - |