Abstract
Although shunt overdrainage is a well-known complication in hydrocephalus management, the problem has been underestimated. Current literature suggests that the topic requires more examination. An insight into this condition is limited by a lack of universally agreed-upon diagnostic criteria, heterogeneity of published series, the multitude of different management options and misunderstanding of relationships among pathophysiological mechanisms involved. We carried out a review of the literature on clinical, radiological, intracranial pressure (ICP), pathophysiological and treatment concepts to finally propose an integrative model. Active prophylaxis and management are proposed according to this model based on determination of pathophysiological mechanisms and predisposing factors behind each individual case. As pathophysiology is progressively multifactorial, prevention of siphoning with gravitational valves or antisiphon devices is mandatory to avoid or minimize further complications. Shunt optimization or transferal and neuroendoscopy may be recommended when ventricular collapse and cerebrospinal fluid isolation appear. Cranial expansion may be useful in congenital or acquired craniocerebral disproportion and shunting the subarachnoid space in communicating venous hydrocephalus and idiopathic intracranial hypertension.
Highlights
Shunt Overdrainage: Reappraisal of the Syndrome and Proposal for an Integrative Model
In 18 patients with normal pressure hydrocephalus (NPH), mean cerebrospinal fluid (CSF) pressure values about −220 mm H2 O for ventriculoperitoneal shunts (VPS) and about −190 mm H2 O for ventriculoarterial shunts (VAS) were obtained in the upright position, these findings being explained by the siphoning action of shunts
Portnoy contributed to this “mechanistic model” by developing an “antisiphon device” (ASD) to prevent siphoning [4,9]
Summary
Historical cases of excessive drainage of brain fluid have been previously reported in the literature [1,2,3,4,5,6,7]. In 1982 Hyde-Rowan and coworkers first defined the so-called “slit ventricle syndrome” (SVS) as the clinical picture characterized by a triad: intermittent or chronic headaches, small ventricles on CT scan or ventriculogram, and slow refill of the palpable valve mechanism These characteristic episodes, usually lasting from 10 to 90 min, were considered to be secondary to ventricular catheter obstruction that was, episodic as well. The five known different categories have been re-named: severe intracranial hypotension or low-pressure headaches (analogous to spinal headaches), intermittent obstruction of the ventricular catheter (“slit ventricle syndrome” itself), intracranial hypertension with small ventricles and a failed shunt, intracranial hypertension with a working shunt and headaches unrelated to shunt function (“shunt-related migraine”) [26] These concepts, which have been globally accepted, include the whole spectrum, so a variety of symptoms, clinical presentations, radiological findings and pressure readings can be expected [28]. In an attempt to confront these limitations, we will consider clinical, radiological, ICP, pathophysiological and treatment concepts separately, to propose an integrative model for the management of shunt overdrainage syndrome (SOS)
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