Acta neurochirurgica · 2020
Hypozincaemia is associated with severity of aneurysmal subarachnoid haemorrhage: a retrospective cohort study.
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Arleth Tobias, Olsen Markus Harboe, Orre Matias, Rasmussen Rune, Bache Søren, Eskesen Vagn, Frikke-Schmidt Ruth, Møller Kirsten
Аннотация
BACKGROUND: Hypozincaemia may develop in critically ill patients, including those with acute brain injury in the early phase after hospital admission. The aim of this study was to investigate the prevalence of hypozincaemia after aneurysmal subarachnoid haemorrhage (aSAH) and its association with delayed cerebral ischemia and functional outcome.
METHODS: We retrospectively analysed a cohort of 384 patients with SAH admitted to the Neurointensive Care Unit at Rigshospitalet, Copenhagen, Denmark, in whom at least one measurement of plasma zinc concentration was done during the hospital stay. Hypozincaemia was defined as at least one measurement of plasma zinc below 10 μmol/L. Potential associations between hypozincaemia, demographic variables and functional outcome after aSAH were analysed in multivariable logistic regression models.
RESULTS: Hypozincaemia was observed in 67% (n = 257) of all patients and occurred within 7 days in more than 95% of all hypozincaemic patients. In a multivariable model, severe SAH (WFNS 3-5; OR 4.2, CI 2.21-8.32, p < 0.001) and Sequential Organ Failure Assessment (SOFA) score on the day of admission (OR 1.24, CI 1.11-1.40, p < 0.001) were independently associated with hypozincaemia. In another multivariable model, hypozincaemia was independently associated with an unfavourable outcome (defined as a modified Rankin Scale score from 3 to 6) (OR 1.97, CI 1.06-3.68, p = 0.032), as was age (OR 1.03, CI 1.01-1.05, p = 0.015), SOFA score on the day of admission (OR 1.14, CI 1.02-1.29, p = 0.02), a diagnosis of delayed cerebral ischaemia (OR 4.06, CI 2.29-7.31, p < 0.001) and a clinical state precluding assessment for delayed cerebral ischaemia (OR 15.13, CI 6.59-38.03, p < 0.001).
CONCLUSION: Hypozincaemia occurs frequently after aSAH, is associated with a higher disease severity and independently contributes to an unfavourable outcome.
METHODS: We retrospectively analysed a cohort of 384 patients with SAH admitted to the Neurointensive Care Unit at Rigshospitalet, Copenhagen, Denmark, in whom at least one measurement of plasma zinc concentration was done during the hospital stay. Hypozincaemia was defined as at least one measurement of plasma zinc below 10 μmol/L. Potential associations between hypozincaemia, demographic variables and functional outcome after aSAH were analysed in multivariable logistic regression models.
RESULTS: Hypozincaemia was observed in 67% (n = 257) of all patients and occurred within 7 days in more than 95% of all hypozincaemic patients. In a multivariable model, severe SAH (WFNS 3-5; OR 4.2, CI 2.21-8.32, p < 0.001) and Sequential Organ Failure Assessment (SOFA) score on the day of admission (OR 1.24, CI 1.11-1.40, p < 0.001) were independently associated with hypozincaemia. In another multivariable model, hypozincaemia was independently associated with an unfavourable outcome (defined as a modified Rankin Scale score from 3 to 6) (OR 1.97, CI 1.06-3.68, p = 0.032), as was age (OR 1.03, CI 1.01-1.05, p = 0.015), SOFA score on the day of admission (OR 1.14, CI 1.02-1.29, p = 0.02), a diagnosis of delayed cerebral ischaemia (OR 4.06, CI 2.29-7.31, p < 0.001) and a clinical state precluding assessment for delayed cerebral ischaemia (OR 15.13, CI 6.59-38.03, p < 0.001).
CONCLUSION: Hypozincaemia occurs frequently after aSAH, is associated with a higher disease severity and independently contributes to an unfavourable outcome.