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Cardiovascular Drugs
Published in Radhwan Nidal Al-Zidan, Drugs in Pregnancy, 2020
Risk Summary: It should be used with caution because the pregnancy experience in humans is limited, and the reproduction studies in animals have shown the risk of teratogenicity associated with the use of Nimodipine.
Cranial Neurosurgery
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Patients should be placed on bed rest with hourly neuro observations. They require strict input-output monitoring and intravenous fluid replacement with normal saline initially. Oral nimodipine at a dose of 60 mg every 4 hours reduces the rate of poor outcome (see Vasospasm below). Analgesics, laxatives, anti-emetics, gastric protection and compression stockings are also likely to be necessary. After resuscitation, the priorities in subarachnoid haemorrhage are:
Effectiveness of nimodipine on non-traumatic subarachnoid hemorrhage based on computed tomography angiography
Published in Elida Zairina, Junaidi Khotib, Chrismawan Ardianto, Syed Azhar Syed Sulaiman, Charles D. Sands, Timothy E. Welty, Unity in Diversity and the Standardisation of Clinical Pharmacy Services, 2017
J. Khotib, S.S. Ganesen, A.F. Sani
Various studies have been conducted to determine the effectiveness of nimodipine drugs in SAH patients. From the 2009 Harsono study, nimodipine is a drug that can pass through the blood–brain barrier and inhibit calcium ions into cells by reducing the contractile state of smooth muscle at depolarization and causing vasoconstriction. The use of nimodipine in vasospasm patients after SAH aneurysms has proved to improve neurological recovery and reduce cerebral infestation. Vergouwen et al. (2006) conducted a randomized study of 1,074 patients with non-traumatic subarachnoid hemorrhage using oral nimodipine compared with placebo to determine the effectiveness of oral nimodipine in reducing cerebral infarction and therapy outcome after subarachnoid hemorrhage.
Percutaneous transluminal angioplasty for radial artery graft stenosis after high-flow superficial temporal artery trunk to middle cerebral artery interposition bypass
Published in British Journal of Neurosurgery, 2023
Chuan Chen, Yang Yang, Cong Ling, Haiyong He, Lun Luo, Hui Wang
After induction of general anaesthesia, nimodipine was continuously administered intravenously. A 6F Envoy guiding catheter (Cordis, Miami Lakes, Florida) was placed at the origin of the right external carotid artery (ECA), and an angiography image showed severe stenosis (>80%) in the RAG at a site 4 mm away from the RA-MCA anastomosis site. After systemic heparinization, a 1.5 × 9 mm Gateway balloon catheter (Boston Scientific) was advanced into the stenotic site guided by a 0.014-inch Traxcess microguidewire (MicroVention Terumo) (ensuring that the balloon tip did not touch the anastomosis site). The balloon was inflated at a speed of 1 atm/10 s and then deflated slowly as soon as it reached the set pressure of 6 atm. Re-examination by angiography showed severe local vasospasm in the RAG. Therefore, the balloon was inflated again at a speed of 1 atm/10 s. After the set pressure was reached, the pressure of the balloon was maintained for 30 s before the balloon was slowly deflated. The expansion process was repeated three more times until the stenosis was <40% (Figure 2). Angiography was performed to confirm the RAG calibre after each expansion. Thirty minutes after completion of PTA, angiography was performed again to confirm the absence of severe vasospasm. After treatment, heparin was neutralized.
Effect of Nimodipine on Macular and Peripapillary Capillary Vessel Density in Patients with Normal-tension Glaucoma Using Optical Coherence Tomography Angiography
Published in Current Eye Research, 2021
Xinxin Hu, Xiaolei Wang, Yi Dai, Chen Qiu, Kunte Shang, Xinghuai Sun
Nimodipine, a blocker of the 1,4-di-hidropyridine calcium channel, prevents the influx of calcium and regulates intracellular calcium concentration.13 Nimodipine has high lipid solubility, easily crosses the blood–brain barrier,14 and is relatively selective for cerebral vessels; hence, it may be suggested as a calcium channel blocker (CCB) for ophthalmic use.15 Nimodipine is known to relieve the pressure on blood vessels by dilating cerebral arteries and arterioles, which increases cerebral blood flow.16 However, the reported effects of nimodipine on ocular blood flow in patients with NTG are controversial. Several investigators have demonstrated that oral administration of nimodipine increases retinal capillary blood flow,17 optic nerve head and choroidal blood flow.12 Conversely, Piltz et al reported that nimodipine had little effect on macular blood flow in patients with NTG.11 However, these trials mainly use the blue field entoptic stimulation technique or laser Doppler flowmetry, which are not sensitive enough to accurately measure the low velocities of blood flow in small vessels.18
Daily systemic energy expenditure in the acute phase of aneurysmal subarachnoid hemorrhage
Published in Upsala Journal of Medical Sciences, 2019
Christoffer Nyberg, Elisabeth Ronne Engström, Lars Hillered, Torbjörn Karlsson
Patients were included from October 2010 until July 2014. Mechanically ventilated patients with spontaneous SAH were considered for inclusion. Twenty-six patients were included with at least two measurements using indirect calorimetry during the first week after SAH. The patients were managed according to the Department of Neurosurgery’s protocols for SAH (15). Briefly, this includes early diagnosis and treatment of aneurysm. Patients with impaired consciousness were intubated and normo-ventilated. A ventricular catheter was placed for drainage of cerebrospinal fluid and monitoring of intracranial pressure. Sedation in mechanically ventilated patients was obtained, mainly with propofol and bolus doses of morphine. Enteral nutrition was administered through a gastro-enteral tube. Intravenous nutrition was only used in selected cases. Nimodipine was administered for three weeks. Symptoms of delayed cerebral ischemia were considered to be due to vasospasm when other causes of deterioration were ruled out. Vasospasm treatment was then given with increase in blood volume and blood pressure and in selected cases intra-arterial administration of nimodipine. Secondary insults putting further strain on the brain’s supply and use of energy and oxygen were systematically detected and treated if present (16). The Uppsala University Regional Ethical Review Board for clinical research granted ethical permission.