Artikel
The venous pathophysiology of chronic overdrainage syndrome
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Veröffentlicht: | 4. Juni 2012 |
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Gliederung
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Objective: The pathophysiology of chronic overdrainage syndrome (COS), or slit ventricle syndrome, is still not universally known or accepted. A venous pathophysiology has been proposed by Sood et al in 2004. We present an educative case-based update highlighting the intracranial dynamics of COS and supporting the venous pathophysiology.
Methods: A 27-year-old women, with years-long history of severe COS attacks (throbbing headaches, nausea/vomiting) requiring each time hospitalization, had small but non-slit ventricles, stable in size during attacks. Only “time-free-of-attacks” was during pregnancy. Patient received computerized ICP-monitoring during attack. Continuous “B-wave-storm” with peak-ICP up to 70 mmHg was recorded, high RAP and ICP-amplitudes indicated lost reserve-capacity. Episode resolved over 8–10 h with parallel stepwise normalization of ICP-parameters. Next evening ICP was -17 mmHg in upright position, taking 2 h to reach 0 mmHg when supine.
Results: Shunt at revision was patent. Patient received programmable-valve at 7 cm H2O for lying-position and programmable gravity-assisted-valve for upright-position (proSA) at 15 cm H2O. Attacks continued until proSA was stepwise raised to 32 cm H2O and never appeared thereafter.
Conclusions: High ICP, RAP and ICP-amplitudes in patient with patent shunt and non-slit ventricles, with unchanged CT and stepwise resolution of symptoms can only be explained by venous entrapment as hypothesized by Sood et. al 2004. Chronic ultra-low CSF-pressures lead to distention of capacity veins, which in turn are more collapsible. Venous collapse leads to sudden blood-entrapment and loss of reserve capacity (high RAP/amplitudes) resulting in ICP crisis. Normalization of ICP during upright-position (pregnancy, proSA) cures COS, probably by normalizing weinsize and collapsibility.