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ABSTRACT: Cerebrospinal fluid (CSF) shunt procedures have dramatically reduced the morbidity and mortality rates associated with hydrocephalus. However, despite improvements in materials, devices, and surgical techniques, shunt failure and complications remain common and may require multiple surgical procedures.
To evaluate CSF shunt complication incidence and factors that may be associated with increased shunt dysfunction and infection rates in adults.
From January 1999 to December 2006, we conducted a prospective surveillance program for all neurosurgical procedures including reoperations and infections. Patients undergoing CSF shunt placement were retrospectively identified among patients labeled in the database as having a shunt as a primary or secondary intervention. Revisions of shunts implanted in another hospital or before the study period were excluded, as well as lumbo- or cyst-peritoneal shunts. Shunt complications were classified as mechanical dysfunction or infection. Follow-up was at least 2 years. Potential risk factors were evaluated using log-rank tests and stepwise Cox regression models.
During the 8-year surveillance period, a total of 14 275 patients underwent neurosurgical procedures, including 839 who underwent shunt placement. One hundred nineteen patients were excluded, leaving 720 study patients. Mechanical dysfunction occurred in 124 patients (17.2%) and shunt infection in 44 patients (6.1%). These 168 patients required 375 reoperations. Risk factors for mechanical dysfunction were atrial shunt, greater number of previous external ventriculostomies, and male sex; risk factors for shunt infection were previous CSF leak, previous revisions for dysfunction, surgical incision after 10 am, and longer operating time.
Shunt surgery still carries a high morbidity rate, with a mean of 2.2 reoperations per patient in 23.3% of patients. Our risk-factor data suggest methods for decreasing shunt-related morbidity, including peritoneal routing whenever possible and special attention to preventing CSF leaks after craniotomy or external ventriculostomy.
Neurosurgery 01/2011; 68(4):985-94; discussion 994-5. · 2.79 Impact Factor
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ABSTRACT: Recent evidence supports a crucial role for matrix metalloproteinase-9 (MMP-9) in blood-brain barrier (BBB) disruption and vasogenic edema formation after traumatic brain injury (TBI). Although the exact causes of MMP-9 upregulation after TBI are not fully understood, several arguments suggest a contribution of the enzyme poly(ADP-ribose)polymerase (PARP) in the neuroinflammatory response leading to MMP-9 activation. The objectives of this study were to evaluate the effect of PARP inhibition by 3-aminobenzamide (3-AB) (1) on MMP-9 upregulation and BBB integrity, (2) on edema formation as assessed by magnetic resonance imaging (MRI), (3) on neuron survival as assessed by (1)H magnetic resonance spectroscopy ((1)H-MRS), and (4) on neurological deficits at the acute phase of TBI. Western blots and zymograms showed blunting of MMP-9 upregulation 6 h after TBI. BBB permeability was decreased at the same time point in 3-AB-treated rats compared to vehicle-treated rats. Cerebral MRI showed less "free" water in 3-AB-treated than in vehicle-treated rats 6 h after TBI. MRI findings 24 h after TBI indicated predominant cytotoxic edema, and at this time point no significant differences were found between 3-AB- and vehicle-treated rats with regard to MMP-9 upregulation, BBB permeability, or MRI changes. At both 6 and 24 h, neurological function was better in the 3-AB-treated than in the vehicle-treated rats. These data suggest that PARP inhibition by 3-AB protected the BBB against hyperpermeability induced by MMP-9 upregulation, thereby decreasing vasogenic edema formation 6 h after TBI. Furthermore, our data confirm the neuroprotective effect of 3-AB at the very acute phase of TBI.
Journal of neurotrauma 04/2010; 27(6):1069-79. · 4.25 Impact Factor
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ABSTRACT: Magnetic resonance imaging (MRI) is widely used to evaluate the consequences of traumatic brain injury (TBI) in both experimental and clinical studies. Improved assessment of experimental TBI using the same methods as those used in clinical investigations would help to translate laboratory research into clinical advances. Here our goal was to characterize lateral fluid percussion-induced TBI, with special emphasis on differentiating the contused cortex from the pericontusional subcortical tissue. We used both in vivo MRI and proton magnetic resonance spectroscopy ((1)H-MRS) to evaluate adult male Sprague-Dawley rats 24 h and 48 h and 7 days after TBI. T2 and apparent diffusion coefficient (ADC) maps were derived from T2-weighted and diffusion-weighted images, respectively. Ratios of N-acetylaspartate (NAA), choline compounds (Cho), and lactate (Lac) over creatine (Cr) were estimated by (1)H-MRS. T2 values were high in the contused cortex 24 h after TBI, suggesting edema development; ADC was low, consistent with cytotoxic edema. At the same site, NAA/Cr was decreased and Lac/Cr elevated during the first week after TBI. In the ipsilateral subcortical area, NAA/Cr was markedly decreased and Lac/Cr was elevated during the first week, although MRI showed no evidence of edema, suggesting that (1)H-MRS detected "invisible" damage. (1)H-MRS combined with MRI may improve the detection of brain injury. Extensive assessments of animal models may increase the chances of developing successful neuroprotective strategies.
Journal of neurotrauma 09/2009; 27(1):85-94. · 4.25 Impact Factor
