Artikel
Is Quantitative Pupillometry (aQP) a suitable monitoring device for detecting increased intracranial pressure?
Korreliert die quantitative Pupillometrie mit dem Anstieg des intrakraniellen Drucks?
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Autoren
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Alexander E. Hartmann
- Kliniken der Stadt Köln, Neurochirurgie, Köln, Deutschland; Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Köln, Deutschland
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Thorsten Annecke
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Köln, Deutschland; Kliniken der Stadt Köln, Anästhesiologie und operative Intensivmedizin, Köln, Deutschland
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Juliane Ruf
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Köln, Deutschland
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Paiman Shalchian-Tehran
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Köln, Deutschland; Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Klinik für Neurochirurgie, Köln, Deutschland
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Makoto Nakamura
- Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Köln, Deutschland; Krankenhaus Köln-Merheim, Klinikum der Universität Witten/Herdecke, Klinik für Neurochirurgie, Köln, Deutschland
| Veröffentlicht: | 25. Mai 2022 |
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Gliederung
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Objective: Pupillary abnormalities may accompany an increase of intracranial pressure (ICP). It has been stated that a decrease of NPI, calculated from multiple parameters of the quantitative pupillary dynamics, is an effective warning sign for increased ICP (Chen et al., Surg Neurol Int, 2011). Our aim was to investigate the time course between NPI and changig ICP and potential correlations between the dynamics of both parameters.
Methods: n= 93 (m/f, adults, SAH, head trauma, ICB, no eye disease), all with direct ICP recording). Stratification with respect to the location of the primary cause of damage (fossa anterior, middle, posterior fossa) and ICP classes.
Consecutive recording of ICP by extraventricular drainage system (EVD) and pupillary dynamics by repetitive bedside automatic quantitative pupillometry (aQP) with documentation of size/velocity of pupillary constriction/dilatation, delay of start of constriction and others. Calculation of NPI has been done using these parameters: normal NPi 3-5; abnormal 0-2,9. Repetitive recordings of aQP over several consecutive days, at least 4 x / 24 hrs. 3 ICP-classes were divided: 0 - 15 mmHg (n-ICP), moderately abnormal 16-30 mmHg (ma-ICP), extremely abnormal above 30 mmHg (ea-ICP).
Results: In 51/93 pts. ICP and NPI were normal. In the remaining 42/93 pts. abnormal ICP or /and aQP with bilateral or right-left difference of pupil size / constriction velocity were observed. In these 42 pts. ICP increased for variable duration. 29/42 pts. presented an abnormal NPI (0-3) in the following ICP classes: n=6 for n-ICP, n=17 for ma-ICP and n=6 for ea-ICP. In 13/42 pts. NPI was normal despite increased ICP, all in the ma-ICP class. Abnormal NPI has been observed more in primary damage of the frontal and temporal fossae than in patients with primary damage in the posterior fossa. Early decrease of NPI below 3 before increase of ICP has been observed in 4 out of the 17 pts.
Conclusion: Measurement of pupil dynamics can not replace the direct recording of ICP. A relation between NPI and ICP changes occur more often in diseases of the anterior and middle fossa than in diseases of the posterior fossa. In high ICP (>30 mmHg) pupillary abnormalities are often observed. Alarming changes of pupillary dynamics prior to monitored ICP increase are a rarity.
