Vasoplegic Syndrome after Oral Nimodipine Application in Patients with Subarachnoid Hemorrhage

doi:10.15406/jaccoa.2014.01.00035

Cited by 3 publications

(2 citation statements)

References 23 publications

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“…In general, CCB-induced vasoplegia is commonly reported as a complication of subarachnoid hemorrhage treatment rather than intentional toxicity. A case series of four patients by Bele S et al was the first to report refractory vasoplegia resulting from nimodipine administration, which was successfully resolved by administering methylene blue [20]. Similarly, Clifford KM et al were pioneers in describing the use of hydroxocobalamin for CCB-induced vasoplegia, which led to a significant increase in MAP within minutes of medication administration [21].…”

Section: Discussionmentioning

confidence: 99%

Hydroxocobalamin as Rescue Therapy in a Patient With Refractory Amlodipine-Induced Vasoplegia

Ayasa¹,

Azar²,

Odeh³

et al. 2023

Cureus

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Vasoplegic syndrome is a type of distributive shock characterized by mean arterial pressure of less than 65 mmHg, with normal to high cardiac output and often refractory to fluid resuscitation, high doses of intravenous vasopressors, and inotropes. It is usually observed after cardiac and solid organ transplantation surgeries.Here, we report a 56-year-old female patient who presented with a profound vasoplegia manifesting as lethargy and confusion in the setting of amlodipine toxicity. This case of severe vasoplegia was refractory to all conditional lines of medical management reported in the literature. The mainstay treatment modalities for vasoplegia include volume resuscitation, catecholamines, vasopressin, angiotensin II, and possibly methylene blue in unresponsive cases. Our patient was given hydroxocobalamin in favor of methylene blue, given the history of serotonin reuptake inhibitors use, which would have caused a life-threatening serotonin syndrome. Hydroxycobolamine resulted in a dramatic clinical recovery, suggesting its potentially significant role in refractory vasoplegia.

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Section: Discussionmentioning

confidence: 99%

Hydroxocobalamin as Rescue Therapy in a Patient With Refractory Amlodipine-Induced Vasoplegia

Ayasa¹,

Azar²,

Odeh³

et al. 2023

Cureus

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“…A literature search revealed an isolated case series describing four cases of vasoplegia after oral nimodipine successfully treated with methylene blue. 3 for glucose-6-phosphate dehydrogenase (G6PD) level was sent. We administered intravenous methylene blue 200 mg over 30 minutes as a salvage therapy.…”

Section: Introductionmentioning

confidence: 99%

Methylene Blue to the Rescue in Severe Vasoplegia after Oral Nimodipine in a Patient with Aneurysmal Subarachnoid Hemorrhage

Ramasubban¹,

Goswami²,

Sharma³

et al. 2023

Indian Journal of Critical Care Case Report

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A 53-year-old man presented with fever, headache, and neck pain for 7 days. Brain computed tomography (CT) done from outside facility was noncontributory. A lumbar puncture was done, and cerebrospinal fluid (CSF) was uniformly hemorrhagic. After correcting for red blood cells, his CSF still had an elevated white blood cell (WBC) count (neutrophilic predominance) and protein level, with a CSF to serum glucose ratio of <0.4. The CSF was negative for tuberculosis and multiplex polymerase chain reaction (PCR) based common pathogens. He was hemodynamically stable. The WBC and C-reactive proteins were marginally elevated. Intravenous ceftriaxone and vancomycin started.

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Beyond nimodipine: advanced neuroprotection strategies for aneurysmal subarachnoid hemorrhage vasospasm and delayed cerebral ischemia

Luzzi,

Bektaşoğlu,

Doğruel

et al. 2024

Neurosurg Rev

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The clinical management of aneurysmal subarachnoid hemorrhage (SAH)-associated vasospasm remains a challenge in neurosurgical practice, with its prevention and treatment having a major impact on neurological outcome. While considered a mainstay, nimodipine is burdened by some non-negligible limitations that make it still a suboptimal candidate of pharmacotherapy for SAH. This narrative review aims to provide an update on the pharmacodynamics, pharmacokinetics, overall evidence, and strength of recommendation of nimodipine alternative drugs for aneurysmal SAH-associated vasospasm and delayed cerebral ischemia. A PRISMA literature search was performed in the PubMed/Medline, Web of Science, ClinicalTrials.gov, and PubChem databases using a combination of the MeSH terms “medical therapy,” “management,” “cerebral vasospasm,” “subarachnoid hemorrhage,” and “delayed cerebral ischemia.” Collected articles were reviewed for typology and relevance prior to final inclusion. A total of 346 articles were initially collected. The identification, screening, eligibility, and inclusion process resulted in the selection of 59 studies. Nicardipine and cilostazol, which have longer half-lives than nimodipine, had robust evidence of efficacy and safety. Eicosapentaenoic acid, dapsone and clazosentan showed a good balance between effectiveness and favorable pharmacokinetics. Combinations between different drug classes have been studied to a very limited extent. Nicardipine, cilostazol, Rho-kinase inhibitors, and clazosentan proved their better pharmacokinetic profiles compared with nimodipine without prejudice with effective and safe neuroprotective role. However, the number of trials conducted is significantly lower than for nimodipine. Aneurysmal SAH-associated vasospasm remains an area of ongoing preclinical and clinical research where the search for new drugs or associations is critical.

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Vasoplegic Syndrome after Oral Nimodipine Application in Patients with Subarachnoid Hemorrhage

Cited by 3 publications

References 23 publications

Hydroxocobalamin as Rescue Therapy in a Patient With Refractory Amlodipine-Induced Vasoplegia

Hydroxocobalamin as Rescue Therapy in a Patient With Refractory Amlodipine-Induced Vasoplegia

Methylene Blue to the Rescue in Severe Vasoplegia after Oral Nimodipine in a Patient with Aneurysmal Subarachnoid Hemorrhage

Beyond nimodipine: advanced neuroprotection strategies for aneurysmal subarachnoid hemorrhage vasospasm and delayed cerebral ischemia

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