Acute and Critical Care

Review Article

Neurosurgery
The role of catecholamines in aneurysmal subarachnoid hemorrhage: a narrative review: Samantha Nalliah, Tariq Janjua, Luis Rafael Moscote-Salazar, Md Yunus, Amit Agrawal; Acute Crit Care. 2025;40(4):513-520. Published online November 24, 2025; DOI: https://doi.org/10.4266/acc.001525

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The marked release of catecholamines during subarachnoid hemorrhage is an important aspect of the pathobiology following aneurysmal rupture. This narrative review aims to identify how catecholamines influence aneurysmal subarachnoid hemorrhage (aSAH) outcomes. aSAH is a critical neurological condition characterized by hemorrhage into the subarachnoid space, leading to severe neurological deficits and mortality. Catecholamines, including epinephrine, norepinephrine, and dopamine, are the body's stress responses, which can lead to secondary injuries following aSAH. This review was conducted through a targeted literature search of relevant studies examining the relationship between aSAH, catecholamines, and clinical outcomes. Searches were performed in PubMed, Scopus, The Cochrane Library, Medline (Ovid), Embase (Ovid), and CINAHL, including publications up to July 2024. Search terms combined keywords and subject headings related to “subarachnoid hemorrhage” or “aSAH,” “catecholamines,” “epinephrine,” “norepinephrine,” “dopamine,” and outcome-related terms such as “prognosis,” “mortality,” and “neurological outcome.” Articles were selected based on relevance, and key findings were synthesized descriptively to provide a comprehensive overview of current knowledge in this area. Elevated levels of catecholamines are observed following aSAH and are associated with increased sympathetic nervous system activity. This catecholamine surge contributes to pathological processes, including vasospasm, blood-brain barrier disruption, cerebral edema, and neuronal damage. The review highlights the implications of catecholamine levels; where higher concentrations correlate with poorer outcomes and higher mortality rates. Understanding the mechanisms responsible for secondary injury due to catecholamines surge following aSAH shall facilitate the development of therapeutic approaches to prevent secondary brain injury and improve outcomes.

Citations

Citations to this article as recorded by

Glucose/Potassium Ratio, a Novel Biomarker for the Prognosis of Patients with Subarachnoid Hemorrhage: A Review
Luis E. Fernández-Garza, Valeria A. Fernández-Garza, Daniela Mares-Custodio, Victor Gutiérrez-Ruano, Alexandro Navarrete-Rodríguez, Juan J. Arias-Alzate
Journal of Vascular Diseases.2025; 4(4): 48. CrossRef

Case Report

Genetic
Lethal Hyperammonemia due to Ornithine Transcarbamylase Deficiency in a Patient with Severe Septic Shock: Ji An Hwang, Joo Han Song, Young Seok Lee, Kyung Soo Chung, Song Yee Kim, Eun Young Kim, Ji Ye Jung, Young Ae Kang, Young Sam Kim, Joon Chang, Moo Suk Park; Korean J Crit Care Med. 2016;31(2):140-145. Published online May 31, 2016; DOI: https://doi.org/10.4266/kjccm.2016.31.2.140

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Abstract PDF

Severe hyperammonemia can occur as a result of inherited or acquired liver enzyme defects in the urea cycle, among which ornithine transcarbamylase deficiency (OTCD) is the most common form. We report a very rare case of a 45-year-old Korean male who was admitted to the intensive care unit (ICU) due to severe septic shock with acute respiratory failure caused by Pneumocystis jiroveci pneumonia. During his ICU stay with ventilator care, the patient suffered from marked hyperammonemia (>1,700 μg/dL) with abrupt mental change leading to life-threatening cerebral edema. Despite every effort including continuous renal replacement therapy and use of a molecular adsorbent recirculating system (extracorporeal liver support–albumin dialysis) to lower his serum ammonia level, the patient was not recovered. The lethal hyperammonemia in the patient was later proven to be a manifestation of acquired liver enzyme defect known as OTCD, which is triggered by serious catabolic conditions, such as severe septic shock with acute respiratory failure.

Citations

Citations to this article as recorded by

Emerging neurological and cognitive symptoms in patients with late-onset ornithine transcarbamylase deficiency: a narrative review
Laura Konczal, Gregory M. Enns, Andrea L. Gropman, Daniel Garcia, J. Lawrence Merritt II, Greta Wilkening
Metabolic Brain Disease.2026;[Epub] CrossRef

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