Effects of Perioperative Indomethacin on Intracranial Pressure, Cerebral Blood Flow, and Cerebral Metabolism in Patients Subjected to Craniotomy for Cerebral Tumors

Bundgaard, Henning; Jensen, Katrine; Cold, Georg E.; Bergholt, Bo; Frederiksen, Ruben; S, Pless

doi:10.1097/00008506-199610000-00003

Cited by 36 publications

(39 citation statements)

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“…The only tomographic study on living animals (Schumann et al, 1996), found no change of the global CMR O 2 but interestingly (see below) a small and significant increase of CMR O 2 in thalamus and pons. In adult humans, the effect of indomethacin on CMR O 2 was assessed only by the arterio-venous difference (Wennmalm et al, 1981;Jensen et al, 1991;Dahl et al, 1996;Bundgaard et al, 1996) and no significant change was observed in any of these studies. However, a study of preterm infants with near-infrared-spectroscopy of cytochrome oxidase indicated reduced oxygenation (Benders et al, 1995).…”

Section: Effect Of Indomethacin On Cmr Omentioning

confidence: 99%

Cerebral Metabolic Response to Low Blood Flow: Possible Role of Cytochrome Oxidase Inhibition

Gjedde

Johannsen

Cold

et al. 2005

J Cereb Blood Flow Metab

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The reactions of cerebral metabolism to imposed changes of cerebral blood flow (CBF) are poorly understood. A common explanation of the mismatched CBF and oxygen consumption (CMR O 2 ) during neuronal excitation holds that blood flow rises more than oxygen consumption to compensate for an absent oxygen reserve in brain mitochondria. The claim conversely implies that oxygen consumption must decline when blood flow declines. As the prevailing rate of reaction of oxygen with cytochrome c oxidase is linked to the tension of oxygen, the claim fails to explain how oxygen consumption is maintained during moderate reductions of CBF imposed by hyperventilation (hypocapnia) or cyclooxygenase (COX) inhibition. To resolve this contradiction, we extended the previously published oxygen delivery model with a term allowing for the adjustment of the affinity of cytochrome c oxidase to a prevailing oxygen tension. The extended model predicted constant oxygen consumption at moderately reduced blood flow. We determined the change of affinity of cytochrome c oxidase in the extended model by measuring CBF in seven, and CMR O 2 in five, young healthy volunteers before and during COX inhbition with indomethacin. The average CBF declined 35%, while neither regional nor average CMR O 2 changed significantly. The adjustment of cytochrome c oxidase affinity to the declining oxygen delivery could be ascribed to a hypothetical factor with several properties in common with nitric oxide.

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Section: Effect Of Indomethacin On Cmr Omentioning

confidence: 99%

Cerebral Metabolic Response to Low Blood Flow: Possible Role of Cytochrome Oxidase Inhibition

Gjedde

Johannsen

Cold

et al. 2005

J Cereb Blood Flow Metab

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“…All studies were prospective studies, with 2 prospective RCT [14,25] and 10 prospective cohort studies [13,[15][16][17][19][20][21][22][23][24].…”

Section: Resultsmentioning

confidence: 99%

“…Three articles [14,17,25] report the use of indomethacin on patients with supratentorial tumors. One study reported the use of indomethacin for patients with idiopathic intracranial hypertension (IIH) [17].…”

Section: Resultsmentioning

confidence: 99%

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Indomethacin for Control of ICP

et al. 2014

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non-English, retrospective studies, no documentation of ICP response to indomethacin, and animal studies. A two-tier filter of references was conducted. First, we screened manuscripts by title and abstract. Second, those references passing the first filter were pulled, and the full manuscript was checked to see if it matched the criteria for inclusion. Two reviewers independently extracted data including population characteristics and treatment characteristics. The strength of evidence was adjudicated using both the Oxford and GRADE methodology. Our search strategy produced a total of 208 citations. Twelve original articles, 10 manuscripts, and 2 meeting proceeding, were considered for the review with all utilizing indomethacin, while documenting ICP in neurological patients. All studies were prospective. Across all studies, there were a total of 177 patients studied, with 152 receiving indomethacin and 25 serving as controls in a variety of heterogeneous studies. All but one study documented a decrease in ICP with indomethacin administration, with both bolus and continuous infusions. No significant complications were described. There currently exists Oxford level 2b, GRADE C evidence to support that indomethacin reduces ICP in the severe TBI population. Similar conclusions in other populations cannot be made at this time. Comments on its impact, on patient outcome, and side effects cannot be made given the available data. At this time, indomethacin for ICP control remains experimental and further prospective study is warranted.

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“…Increased ICP (ICP>10 mmHg) may cause herniation and cerebral swelling (Bundgaard et al 1998), which increase the risk of cerebral ischaemia with low cerebral perfusion pressure (CPP) (Bundgaard et al 1996). The treatment of increased ICP is one of the most important issues in neurosurgery.…”

Section: Discussionmentioning

confidence: 99%

Systematic review of decreased intracranial pressure with optimal head elevation in postcraniotomy patients: a meta‐analysis

Jiang

You

et al. 2015

Journal of Advanced Nursing

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Effects of Perioperative Indomethacin on Intracranial Pressure, Cerebral Blood Flow, and Cerebral Metabolism in Patients Subjected to Craniotomy for Cerebral Tumors

Cited by 36 publications

References 0 publications

Cerebral Metabolic Response to Low Blood Flow: Possible Role of Cytochrome Oxidase Inhibition

Cerebral Metabolic Response to Low Blood Flow: Possible Role of Cytochrome Oxidase Inhibition

Indomethacin for Control of ICP

Systematic review of decreased intracranial pressure with optimal head elevation in postcraniotomy patients: a meta‐analysis

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