Is Decompressive Craniectomy a Risk Factor for Ventriculomegaly?

OBJECTIVETraumatic intracerebral hemorrhage (TICH) represents approximately 13%–48% of the lesions after a traumatic brain injury (TBI), and hemorrhagic progression (HP) occurs in 38%–63% of cases. In previous studies, decompressive craniectomy (DC) has been characterized as a risk factor in the HP of TICH; however, few studies have focused exclusively on this relationship. The object of the present study was to analyze the relationship between DC and the growth of TICH and to reveal any correlation with the size of the craniectomy, degree of cerebral parenchymal herniation (CPH), or volumetric expansion of the TICH.METHODSThe authors retrospectively analyzed the records of 497 adult patients who had been consecutively admitted after suffering a severe or moderate closed TBI. An inclusion criterion was presentation with one or more TICHs on the initial or control CT. Demographic, clinical, radiological, and treatment variables were assessed for associations.RESULTSTwo hundred three patients presenting with 401 individual TICHs met the selection criteria. TICH growth was observed in 281 cases (70.1%). Eighty-two cases (20.4%) underwent craniectomy without TICH evacuation. In the craniectomy group, HP was observed in 71 cases (86.6%); in the noncraniectomy group (319 cases), HP occurred in 210 cases (65.8%). The difference in the incidence of HP between the two groups was statistically significant (OR 3.41, p < 0.01). The mean area of the craniectomy was 104.94 ± 27.5 cm2, and the mean CPH distance through the craniectomy was 17.85 ± 11.1 mm. The mean increase in the TICH volume was greater in the groups with a craniectomy area > 115 cm2 and CPH > 25 mm (16.12 and 14.47 cm3, respectively, p = 0.01 and 0.02). After calculating the propensity score (PS), the authors followed three statistical methods—matching, stratification, and inverse probability treatment weighting (IPTW)—thereby obtaining an adequate balance of the covariates. A statistically significant relationship was found between HP and craniectomy (OR 2.77, p = 0.004). This correlation was confirmed with the three methodologies based on the PS with odds greater than 2.CONCLUSIONSDC is a risk factor for the growth of TICH, and there is also an association between the size of the DC and the magnitude of the volume increase in the TICH.

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Post-Traumatic Hydrocephalus after Decompressive Craniectomy: An Underestimated Risk Factor

Journal of Neurotrauma ◽

10.1089/neu.2010.1425 ◽

2010 ◽

Vol 27 (11) ◽

pp. 1965-1970 ◽

Cited By ~ 91

Author(s):

Pasquale De Bonis ◽

Angelo Pompucci ◽

Annunziato Mangiola ◽

Luigi Rigante ◽

Carmelo Anile

Keyword(s):

Risk Factor ◽

Decompressive Craniectomy ◽

Post Traumatic

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Complications following pediatric cranioplasty after decompressive craniectomy: a multicenter retrospective study

Journal of Neurosurgery Pediatrics ◽

10.3171/2018.3.peds17234 ◽

2018 ◽

Vol 22 (3) ◽

pp. 225-232 ◽

Cited By ~ 15

Author(s):

Brandon G. Rocque ◽

Bonita S. Agee ◽

Eric M. Thompson ◽

Mark Piedra ◽

Lissa C. Baird ◽

...

Keyword(s):

Risk Factors ◽

Risk Factor ◽

Bone Resorption ◽

Bone Graft ◽

Decompressive Craniectomy ◽

Significant Risk ◽

Retrospective Case ◽

Vp Shunt ◽

Selection Of Variables ◽

Cranial Implant

OBJECTIVEIn children, the repair of skull defects arising from decompressive craniectomy presents a unique set of challenges. Single-center studies have identified different risk factors for the common complications of cranioplasty resorption and infection. The goal of the present study was to determine the risk factors for bone resorption and infection after pediatric cranioplasty.METHODSThe authors conducted a multicenter retrospective case study that included all patients who underwent cranioplasty to correct a skull defect arising from a decompressive craniectomy at 13 centers between 2000 and 2011 and were less than 19 years old at the time of cranioplasty. Prior systematic review of the literature along with expert opinion guided the selection of variables to be collected. These included: indication for craniectomy; history of abusive head trauma; method of bone storage; method of bone fixation; use of drains; size of bone graft; presence of other implants, including ventriculoperitoneal (VP) shunt; presence of fluid collections; age at craniectomy; and time between craniectomy and cranioplasty.RESULTSA total of 359 patients met the inclusion criteria. The patients’ mean age was 8.4 years, and 51.5% were female. Thirty-eight cases (10.5%) were complicated by infection. In multivariate analysis, presence of a cranial implant (primarily VP shunt) (OR 2.41, 95% CI 1.17–4.98), presence of gastrostomy (OR 2.44, 95% CI 1.03–5.79), and ventilator dependence (OR 8.45, 95% CI 1.10–65.08) were significant risk factors for cranioplasty infection. No other variable was associated with infection.Of the 240 patients who underwent a cranioplasty with bone graft, 21.7% showed bone resorption significant enough to warrant repeat surgical intervention. The most important predictor of cranioplasty bone resorption was age at the time of cranioplasty. For every month of increased age the risk of bone flap resorption decreased by 1% (OR 0.99, 95% CI 0.98–0.99, p < 0.001). Other risk factors for resorption in multivariate models were the use of external ventricular drains and lumbar shunts.CONCLUSIONSThis is the largest study of pediatric cranioplasty outcomes performed to date. Analysis included variables found to be significant in previous retrospective reports. Presence of a cranial implant such as VP shunt is the most significant risk factor for cranioplasty infection, whereas younger age at cranioplasty is the dominant risk factor for bone resorption.

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Clinical aspects of reactive oxygen and nitrogen species

Biochemical Society Symposium ◽

10.1042/bss0710121 ◽

2004 ◽

Vol 71 ◽

pp. 121-133 ◽

Cited By ~ 25

Author(s):

Ascan Warnholtz ◽

Maria Wendt ◽

Michael August ◽

Thomas Münzel

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Risk Factor ◽

Endothelial Dysfunction ◽

Vascular Tissue ◽

Rapid Development ◽

Reactive Oxygen ◽

Clinical Aspects ◽

No Production ◽

Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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