The effects of dexmedetomidine on early stage renal functions in pediatric patients undergoing cardiac angiography using non‐ionic contrast media: a double‐blind, randomized clinical trial

Bayram, Adnan; Ülgey, Ayşe; Baykan, Ali; Narın, Nazmi; Narin, Figen; Esmaoğlu, Aliye; Boyacı, Adem

doi:10.1111/pan.12348

Cited by 28 publications

(27 citation statements)

References 23 publications

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“…The use of dexmedetomidine for the pre vention of AKI of diverse etiologies, including CAAKI, has been championed by a Turkish group. Bayram et al 45) analyzed the effect of dexmedetomidine in a randomized, controlled trial (RCT) involving 60 children with CHD, scheduled for coronary angiography. The authors observed CAAKI (pRIFLE criteria) in 3 patients (10%) in the inter vention arm and in 11 (36.7%) in the control arm.…”

Section: Pharmacologic Strategiesmentioning

confidence: 99%

Contrast-Associated Acute Kidney Injury (CA-AKI) in Children: Special Considerations

Windpessl¹,

Kronbichler²

2019

Child Kidney Dis

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Contrast-associated acute kidney injury (CA-AKI) is a major concern when iodinated contrast material is administered, especially in patients at risk. Efforts have been undertaken to understand the detrimental effects of contrast media (CM). With the use of low-osmolar or iso-osmolar CM the incidence of CA-AKI has steadily decreased within the past decade; however, especially in the pediatric population information is scarce. Incidence rates have been reported to range between 0% to 18.75%, particularly depending on indication, selection of population (i.e. preexisting co-morbidities), and definition of AKI. Different biomarkers have been proposed, but confirmatory studies are either lacking or have contributed to their lack of diagnostic power. Proteomic approaches have been employed and may pave the way to such discovery. Prevention strategies have been tested and proposed, but the recently published AMACING and PRESERVE trials have shown that commonly used strategies (such as systematic hydration or administration of N-acetylcysteine) have no role in the prevention of CA-AKI. We propose that thoughtful assessment of one's fluid state is the most appropriate approach and depending on the hydration status diuretics or fluid administration should be provided to achieve an euvolemic state ahead of contrast exposure.

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Section: Pharmacologic Strategiesmentioning

confidence: 99%

Contrast-Associated Acute Kidney Injury (CA-AKI) in Children: Special Considerations

Windpessl¹,

Kronbichler²

2019

Child Kidney Dis

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“…DEX has potential neuroprotective effects [11], especially on the hypoxia-damaged brain. The use of DEX during paediatric angiography prevents renal damage caused by contrast medium, resulting from limited increases in the levels of vasoconstricting substances, endothelin-1 and rennin [12].Our observations reveal that DEX can be a valuable supplement of sedation with other agents, when their action is insufficient; more importantly, it can replace opioids, when they are no longer needed and there is a risk of a patient's adverse reactions to their withdrawal. Since DEX does not…”

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confidence: 80%

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confidence: 99%

Zastosowanie deksmedetomidyny w intensywnej terapii dziecięcej

Piotrowski¹,

Gach²,

Wiszniewski³

2015

Anaesthesiol Intensive Ther

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Sir, In recent years, there has been increased interest in dexmedetomidine (DEX), in both anaesthesiology and intensive care [1]. This alpha-2 receptor agonist has been implicated as the drug of choice for sedation of children after cardiac surgery [2], which is undoubtedly associated with its lack of depressive effects, moderate sedative and analgesic action and beneficial antiarrhythmic effects.We would like to share our experiences with this drug, which has been used in the Paediatric Intensive Care Unit since 2013 after the approval by the hospital therapeutic committee. Until June 2014, dexmedetomidine (Dexdor, Orion Pharma, Espoo, Finland) was used 38 times in 33 children with respiratory failure, as an infusion in an initial dose of 0.5−1.4 µg kg -1 h -1 . The drug was administered to discontinue the supply of earlier agents (mainly opioids) during weaning from a ventilator or to change the mode of sedation. During treatment, the following parameters were recorded: heart rate, respiration rate, SpO 2, arterial pressure (invasive or non-invasive method). Moreover, diuresis and parameters of acid-base balance were monitored. Changes in parameters exceeding 20% of the baseline value were considered adverse. The data are presented in Table 1.The drug was administered as follows: postoperatively in 12 children; during pneumonia treatment -6 children; after injuries -2 children; sepsis -2 children; bronchopulmonary dysplasia -2 children; and, comprising 1 case each, bronchiolitis, airway burns, congenital heart defect, cardiomyopathy, pulmonary hypertension, toxic epidermal necrolysis (Lyell's syndrome), spinal muscular atrophy, encephalopathy and intracranial haemorrhage. Although in 8 cases, DEX was the only sedative used, in other cases, it was an element of multi-drug sedation: midazolam was used in 22 children, morphine in 15, propofol in 14, ketamine in 4, magnesium sulphate in 2, along with fentanyl, clonazepam, fenobarbital and clonidine, comprising 1 case each. After the inclusion of DEX, morphine was discontinued in 11 cases and mechanical ventilation was successfully completed in 9 children. In total, during DEX infusion, ventilation was discontinued and trachea extubated in 24 children (63%) (following completion of earlier infusions of opioids and other sedatives). In 3 children, DEX was discontinued due to no beneficial effects. In 2 children, a decrease in the heart rate by 20% of the baseline value was observed. Bradycardia subsided after a dose reduction or withdrawal of the drug. One patient died during DEX treatment, an event which was unrelated to its use, the cause of death being acute myeloid leukemia and intracranial haemorrhage. One child mistakenly received too high a dose of DEX (8.6 then 4.3 µg kg -1 h -1 ), for 11 days in total. Nonetheless, no cardiovascular disorders or other adverse effects, including withdrawal symptoms, were observed.Initially, DEX was recommended for sedation lasting maximum 24 h; currently, its longer use has also been reported, even for many weeks in the dose...

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“…In addition, the serum creatinine does not accurately depict kidney function until stead-state equilibrium, which can take several days. Neutrophil gelatinase-associated lipocalin (NGAL) in urine and plasma, 2 hr after contrast administration have been shown to be predictive biomarkers of CIN [18] but these results remain unvalidated [19]. Biomarkers such as NGAL could allow for earlier identification and intervention to avoid bad outcomes associated with CIN.…”

Section: Prevention Strategiesmentioning

confidence: 99%

“…Clonidine and dexmedetomidine have been shown in mice to protect against CIN presumably by decreasing regional vascular resistance with increased medullary blood flow [42]. In a randomized prospective double-blinded study of 60 children undergoing cardiac angiography, CIN occurred in only 10% of children who received dexmedetomidine compared to 37% of the controls [19]. The beneficial effect of dexmedetomidine may be due to its preventive effect on the release of vasoconstrictor agents such as endothelin and renin but since this study was restricted to low-risk patients, the results cannot be generalized.…”

Section: Alpha-2-receptor Agonistsmentioning

confidence: 99%

Contrast nephropathy in children

Verghese

2015

J Pediatr Intensive Care

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Contrast-induced nephropathy (CIN) remains a common and potentially serious complication in at risk patients after exposure to contrast agents. Risk factors for CIN include chronic kidney disease, hypotension, diabetes mellitus, recent previous exposure to contrast and all of these are potentially additive. Therefore, careful pre-procedural risk stratification is important. In high-risk patients, contrast should be avoided if possible. If avoidance is not possible, the volume of contrast should be minimized and the type of contrast used should if possible be non-ionic iso-osmolar contrast. In view of the clinical importance of CIN, numerous potential risk-reduction strategies have been evaluated. Adequate intravenous volume expansion with isotonic crystalloid (1.0?1.5 mL/kg per hr) for 3?12 hr before the procedure and continued for 6?24 hr afterward can lessen the probability of CIN in patients at risk. But there are insufficient data on oral fluids as a preventive strategy. Nephrotoxic drugs should be withdrawn before contrast administration in patients at risk for CIN. No adjunctive medical or mechanical treatment has been proved to be efficacious in reducing risk for CIN including prophylactic hemodialysis and hemofiltration, N-acetylcysteine, fenoldopam, dopamine, calcium channel blockers, atrial natriuretic peptide, and L-arginine. The CIN Consensus Working Panel considered that, of the pharmacologic agents that have been evaluated, theophylline, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), ascorbic acid, and prostaglandin E deserve further evaluation.

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The effects of dexmedetomidine on early stage renal functions in pediatric patients undergoing cardiac angiography using non‐ionic contrast media: a double‐blind, randomized clinical trial

Abstract: Dexmedetomidine may be beneficial in protecting against contrast-induced nephropathy during pediatric angiography by preventing the elevation of vasoconstrictor agents such as plasma endothelin-1 and renin.

Cited by 28 publications

References 23 publications

Contrast-Associated Acute Kidney Injury (CA-AKI) in Children: Special Considerations

Contrast-Associated Acute Kidney Injury (CA-AKI) in Children: Special Considerations

Zastosowanie deksmedetomidyny w intensywnej terapii dziecięcej

Contrast nephropathy in children

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