# Prehospital intensive blood pressure management in intracerebral hemorrhage: current evidence, controversies, and future directions

**Authors:** Quan Liu, Sijia Liu, Jialin Yang, Jianfei Wang, Ling Li, Xiaoya Wu, Qing He

PMC · DOI: 10.3389/fmed.2026.1725724 · Frontiers in Medicine · 2026-02-09

## TL;DR

This paper reviews prehospital blood pressure management for brain hemorrhage, highlighting strategies to reduce bleeding and improve outcomes.

## Contribution

The paper provides a synthesis of current evidence and identifies controversies in prehospital ICH management.

## Key findings

- Lowering systolic BP to <140 mmHg within two hours may limit hematoma growth.
- Glyceryl trinitrate showed no benefit and potential harm in some trials.
- Mobile stroke units offer faster treatment but face cost and scalability issues.

## Abstract

Spontaneous intracerebral hemorrhage (ICH) is a severe neurological emergency. Early hematoma expansion(HE), a key modifiable outcome predictor, occurs in approximately 38% of cases. This review synthesizes evidence on prehospital intensive blood pressure (BP) management. Reducing systolic BP to <140 mmHg within two hours of onset limits hematoma growth and may improve functional outcomes. However, the INTERACT-4 trial revealed risks in misdiagnosed ischemic stroke, underscoring the need for accurate prehospital subtyping. RIGHT-2 and MR ASAP trials showed no benefit and potential harm with glyceryl trinitrate (GTN). Mobile stroke units enable faster treatment but face cost and scalability barriers. Controversies persist over optimal BP targets, timing, and patient selection. Future directions include developing “Code ICH” pathways, establishing individualized BP targets, and prospectively validating precision medicine approaches.

## Linked entities

- **Chemicals:** glyceryl trinitrate (PubChem CID 4510)
- **Diseases:** intracerebral hemorrhage (MONDO:0013792), ischemic stroke (MONDO:1060198)

## Full-text entities

- **Genes:** S100B (S100 calcium binding protein B) [NCBI Gene 6285] {aka NEF, S100, S100-B, S100beta}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, UCHL1 (ubiquitin C-terminal hydrolase L1) [NCBI Gene 7345] {aka HEL-117, HEL-S-53, NDGOA, PARK5, PGP 9.5, PGP9.5}, AVP (arginine vasopressin) [NCBI Gene 551] {aka ADH, ARVP, AVP-NPII, AVRP, VP}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}
- **Diseases:** ischemia (MESH:D007511), neurological (MESH:D009461), Stroke (MESH:D020521), cerebral edema (MESH:D001929), ST-Segment Elevation Myocardial Infarction (MESH:D000072657), neurological emergency (MESH:D004630), hemorrhage (MESH:D006470), traumatic brain injury (MESH:D000070642), BBB disruption (MESH:C536830), edema (MESH:D004487), neuroinflammation (MESH:D000090862), neurotoxicity (MESH:D020258), inflammatory (MESH:D007249), cerebral hypoperfusion (MESH:D002547), HE (MESH:D006406), neurological deterioration (MESH:D009422), Coma (MESH:D003128), ATACH-2 (MESH:D020803), toxicity (MESH:D064420), coagulation impairment (MESH:D025861), coagulopathy (MESH:D001778), ischemic stroke (MESH:D002544), brain injury (MESH:D001930), hypertension (MESH:D006973), ICH (MESH:D002543)
- **Chemicals:** nitric oxide (MESH:D009569), glutamate (MESH:D018698), urapidil (MESH:C015568), GTN (MESH:D005996), ASAP (MESH:C070385)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12926355/full.md

## References

60 references — full list in the complete paper: https://tomesphere.com/paper/PMC12926355/full.md

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Source: https://tomesphere.com/paper/PMC12926355