Effects of Calcium and Magnesium Ions on the Systemic and Local Toxicities of the N-Methyl-Glucamine (Meglumine) Salt of Metriozoic Acid (Isopaque)

Salvesen, Sigbjørn; Nilsen, Per Lund; Holtermann, Hugo

doi:10.1080/05678066709170596

Cited by 9 publications

(6 citation statements)

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“…uchiyama et al 33 found elevated concentration of CSF iodine in their index case and not in 4 control cases, supporting evidence of a temporary breakdown of the blood-brain barrier. The cause of the blood brain barrier disruption is variably attributed to the hyperosmolality and chemotoxicity of contrast media 2,16,21,28,[43][44][45][46][47][48][49][50][51][52][53][54][55][56] . Studies suggest that contrast media penetrates the blood-brain barrier as a function of dosage, contact time, concentration of anions in the material, and lipophilic…”

Section: Resultsmentioning

confidence: 99%

Persistent Neurological Deficit from Iodinated Contrast Encephalopathy following Intracranial Aneurysm Coiling

Leong

Fanning²

2012

Interv Neuroradiol

109

148

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Neurotoxicity from iodinated contrast agents is a known but rare complication of angiography and neurovascular intervention. Neurotoxicity results from contrast penetrating the blood-brain barrier with resultant cerebral oedema and altered neuronal excitability. Clinical effects include encephalopathy, seizures, cortical blindness and focal neurological deficits. Contrast induced encephalopathy is extensively reported as a transient and reversible phenomenon. We describe a patient with a persistent motor deficit due to an encephalopathy from iodinated contrast media administered during cerebral aneurysm coiling. This observation and a review of the literature highlights that contrast-induced encephalopathy may not always have a benign outcome and can cause permanent deficits. This potential harmful effect should be recognised by the angiographer and the interventionalist.

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Section: Resultsmentioning

confidence: 99%

Persistent Neurological Deficit from Iodinated Contrast Encephalopathy following Intracranial Aneurysm Coiling

Leong

Fanning²

2012

Interv Neuroradiol

109

148

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“…This effect is attributed to the calcium chelating agents such as sodium citrate and disodium edetate in the CM (Caulfield et al., 1975). It has been shown that addition of calcium to CM reduces the local and systemic effects of CM (Salvesen et al., 1967; Tragardh et al., 1975; Thomson et al., 1978). Modified Renografin prepared with addition of calcium chloride dihydrate decreased the ventricular fibrillation significantly resulting from neutralization or binding of the chelating agents (Thomson et al., 1978).…”

Section: Discussionmentioning

confidence: 99%

Effects of Hyperosmolar Ionic and Low Osmolar Non‐ionic Contrast Media on Acid Base, Blood Gas and Electrolyte Status in Dogs

Izci

Oğurtan

Ceylan

2004

Journal of Veterinary Medicine Series A

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The dogs in groups I, II and III in equal numbers received diatrizoate, iohexol and ioxilan at a dose of 700 mgI/kg intravenously (i.v.) as a bolus, respectively. Blood samples were collected prior to contrast media (CM) administration and thereafter at 3, 15, 30, 60, 90 and 180 min to evaluate acid-base, venous blood gas status (pH, PCO2, PO2, HCO, BE, O2) and electrolytes (Na+, Ca++, K+). Values of pH, PCO2, BE, HCO, Na+ and K+ remained unchanged or within non-significant fluctuations compared with the baseline values. PO2 was significantly different from the baseline values in group 1 up to 90 min after administration, significant alterations were found for O2 saturation in group 1 up to 90 min, and in group II at 3, 60 and 180 min; and for Ca++ in group 1 at all time points except at 90 min, and groups II and II at 3 and 15 min post administration. It was concluded that none of the CM are considered to cause long-lasting and major effects on acid-base, blood gas and electrolyte status.

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“…Half were female. Median BMI was 28.5 kg/m 2 (range [22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41]. All patients had risk factors for microvascular disease, including HTN (n = 6), dyslipidemia (n = 5), CKD (n = 5), prior ischemic stroke (n = 3), connective tissue disorders (n = 2; polycystic kidney disease and fibromuscular dysplasia, respectively) and prior open cranial or neuroendovascular surgery (n = 2).…”

Section: Baseline Patient Characteristicsmentioning

confidence: 99%

Contrast-Induced Encephalopathy and the Blood-Brain Barrier

Maclean,

Rogers,

Muradov

et al. 2024

Can. J. Neurol. Sci.

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Background: Contrast-induced encephalopathy (CIE) is an adverse event associated with diagnostic and therapeutic endovascular procedures. Decades of animal and human research support a mechanistic role for pathological blood-brain barrier dysfunction (BBBd). Here, we describe an institutional case series and review the literature supporting a mechanistic role for BBBd in CIE. Methods: A literature review was conducted by searching MEDLINE, Web of Science, Embase, CINAHL and Cochrane databases from inception to January 31, 2022. We searched our institutional neurovascular database for cases of CIE following endovascular treatment of cerebrovascular disease during a 6-month period. Informed consent was obtained in all cases. Results: Review of the literature revealed risk factors for BBBd and CIE, including microvascular disease, pathological neuroinflammation, severe procedural hypertension, iodinated contrast load and altered cerebral blood flow dynamics. In our institutional series, 6 of 52 (11.5%) of patients undergoing therapeutic neuroendovascular procedures developed CIE during the study period. Four patients were treated for ischemic stroke and two patients for recurrent cerebral aneurysms. Mechanical stenting or thrombectomy were utilized in all cases. Conclusion: In this institutional case series and literature review of animal and human data, we identified numerous shared risk factors for CIE and BBBd, including microvascular disease, increased procedure length, large contrast volumes, severe intraoperative hypertension and use of mechanical devices that may induce iatrogenic endothelial injury.

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Effects of Calcium and Magnesium Ions on the Systemic and Local Toxicities of the N-Methyl-Glucamine (Meglumine) Salt of Metriozoic Acid (Isopaque)

Cited by 9 publications

References 0 publications

Persistent Neurological Deficit from Iodinated Contrast Encephalopathy following Intracranial Aneurysm Coiling

Persistent Neurological Deficit from Iodinated Contrast Encephalopathy following Intracranial Aneurysm Coiling

Effects of Hyperosmolar Ionic and Low Osmolar Non‐ionic Contrast Media on Acid Base, Blood Gas and Electrolyte Status in Dogs

Contrast-Induced Encephalopathy and the Blood-Brain Barrier

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