Samuels R, McGirt MJ, Attenello FJ, Garcés Ambrossi GL, Singh N, Solakoglu C, Weingart JD, Carson BS, Jallo GI. (2009) Incidence of symptomatic retethering after surgical management of pediatric tethered cord syndrome with or without duraplasty. Child's Nervous System. 2009 May 6.
Department of Neurosurgery, Johns Hopkins School of Medicine, 600 N Wolfe Street, Meyer 8-161, Baltimore, MD, 21287, USA.
BACKGROUND: Cord retethering and other postoperative complications can occur after the surgical untethering of a first-time symptomatic tethered cord. It is unclear if using duraplasty vs. primary dural closure in the initial operation is associated with decreased incidence of either immediate postoperative complications or subsequent symptomatic retethering. It is also unclear if different etiologies are associated with different outcomes after each method of closure. We reviewed our pediatric experience in first-time surgical untethering of symptomatic tethered cord syndrome (TCS) to identify the incidence of postoperative complications and symptomatic retethering after duraplasty vs. primary closure.
MATERIALS AND METHODS: We retrospectively reviewed 110 consecutive pediatric (<18 years old) cases of first-time symptomatic spinal cord untethering at our institution over a 10-year period. Incidence of postoperative complications and symptomatic retethering were compared in cases with duraplasty vs. primary dural closure use.
RESULTS: Mean age was 5.7 +/- 4.8 years old. "Complex" etiologies included lipomyelomeningocele or prior lipomyelomeningocele repair in 22 (20%) patients, prior myelomeningocele repair in 35 (32%), and concurrent lumbosacral lipoma in 18 (16%). "Noncomplex etiologies" included fatty filum in 26 (24%) and split cord malformation in five (4%). Seventy-five (68%) cases underwent primary dural closure vs. 35 (32%) with duraplasty. Twenty-nine (26%) patients experienced symptomatic retethering at a median [interquartile range (IQR)] of 30.5 [20.75-41.75] months postoperatively. There was no difference in incidence of postoperative cerebrospinal fluid leak, surgical site infection, or median [IQR] length of stay in patients receiving primary dural closure [4 (5%), 7 (9%), and 5 (4-6) days, respectively] vs. duraplasty [3 (9%), 3 (9%), and 6 [5-8] days, respectively], p > 0.05. Complex etiologies were more likely to retether than noncomplex etiologies after primary closure (33.6% vs. 6.6%, p = 0.05) but not after duraplasty (13.7% vs. 5.4%, p = 0.33). Duraplasty graft type (polytetrafluoroethylene vs. bovine pericardium) was not associated with pseudomeningocele or retethering.
CONCLUSION: In our experience, the increased rate of symptomatic retethering observed with complex pediatric TCS (pTCS) etiologies after primary dural closures was not observed when duraplasty was instituted. Expansile duraplasty may be valuable specifically in the management of patient subgroups with complex pTCS etiologies.
PMID: 19418057
Showing posts with label Treatment. Show all posts
Showing posts with label Treatment. Show all posts
Friday, July 3, 2009
Early results of the Ponseti method for the treatment of clubfoot associated with myelomeningocele.
Gerlach DJ, Gurnett CA, Limpaphayom N, Alaee F, Zhang Z, Porter K, Kirchhofer M, Smyth MD, Dobbs MB. (2009) Early results of the Ponseti method for the treatment of clubfoot associated with myelomeningocele. Journal of Bone and Joint Surgery 2009 Jun;91(6):1350-9.
Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis Shriners Hospital for Children, St. Louis, MO 63110, USA.
BACKGROUND: Myelomeningocele is a common birth defect that is often accompanied by clubfoot deformity. Treatment of clubfoot associated with myelomeningocele traditionally has consisted of extensive soft-tissue release operations, which are associated with many complications. The purpose of the present study was to evaluate the early results of the Ponseti method for the treatment of clubfoot associated with myelomeningocele.
METHODS: Sixteen consecutive patients with myelomeningocele (twenty-eight clubfeet) and twenty consecutive patients with idiopathic clubfeet (thirty-five clubfeet) were followed prospectively while being managed with the Ponseti method. The average duration of follow-up was thirty-four months for the myelomeningocele group and thirty-seven months for the idiopathic group. Clubfoot severity was graded at the time of presentation with use of the Diméglio system. The initial correction that was achieved, casting and/or bracing difficulties, recurrences, and subsequent treatments were evaluated and compared between the two cohorts by means of appropriate statistical analysis.
RESULTS: Eleven (39%) of the twenty-eight clubfeet in the myelomeningocele group were graded as Diméglio grade IV, compared with only four (11%) of the thirty-five clubfeet in the idiopathic group (p = 0.014). Initial correction was achieved in thirty-five clubfeet (100%) in the idiopathic group and in twenty-seven clubfeet (96.4%) in the myelomeningocele group (p = 0.16). Relapse of deformity was detected in 68% of the feet in the myelomeningocele group, compared with 26% of the feet in the idiopathic group (p = 0.001). Relapses were treated successfully without the need for extensive soft-tissue release surgery for all but four of the clubfeet in the myelomeningocele group and for all but one of the clubfeet in the idiopathic group (p = 0.16).
CONCLUSIONS: Our data support the use of the Ponseti method for the initial treatment of clubfoot deformity associated with myelomeningocele, although attention to detail is crucial in order to avoid complications. Longer follow-up will be necessary to assess the risk of late recurrence and the potential need for more extensive clubfoot corrective surgery in this patient population.
PMID: 19487512
Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis Shriners Hospital for Children, St. Louis, MO 63110, USA.
BACKGROUND: Myelomeningocele is a common birth defect that is often accompanied by clubfoot deformity. Treatment of clubfoot associated with myelomeningocele traditionally has consisted of extensive soft-tissue release operations, which are associated with many complications. The purpose of the present study was to evaluate the early results of the Ponseti method for the treatment of clubfoot associated with myelomeningocele.
METHODS: Sixteen consecutive patients with myelomeningocele (twenty-eight clubfeet) and twenty consecutive patients with idiopathic clubfeet (thirty-five clubfeet) were followed prospectively while being managed with the Ponseti method. The average duration of follow-up was thirty-four months for the myelomeningocele group and thirty-seven months for the idiopathic group. Clubfoot severity was graded at the time of presentation with use of the Diméglio system. The initial correction that was achieved, casting and/or bracing difficulties, recurrences, and subsequent treatments were evaluated and compared between the two cohorts by means of appropriate statistical analysis.
RESULTS: Eleven (39%) of the twenty-eight clubfeet in the myelomeningocele group were graded as Diméglio grade IV, compared with only four (11%) of the thirty-five clubfeet in the idiopathic group (p = 0.014). Initial correction was achieved in thirty-five clubfeet (100%) in the idiopathic group and in twenty-seven clubfeet (96.4%) in the myelomeningocele group (p = 0.16). Relapse of deformity was detected in 68% of the feet in the myelomeningocele group, compared with 26% of the feet in the idiopathic group (p = 0.001). Relapses were treated successfully without the need for extensive soft-tissue release surgery for all but four of the clubfeet in the myelomeningocele group and for all but one of the clubfeet in the idiopathic group (p = 0.16).
CONCLUSIONS: Our data support the use of the Ponseti method for the initial treatment of clubfoot deformity associated with myelomeningocele, although attention to detail is crucial in order to avoid complications. Longer follow-up will be necessary to assess the risk of late recurrence and the potential need for more extensive clubfoot corrective surgery in this patient population.
PMID: 19487512
Monday, June 29, 2009
Botulinum toxin-A (Botox) intradetrusor injections in children with neurogenic detrusor overactivity/neurogenic overactive bladder: a systematic liter
Gamé X, Mouracade P, Chartier-Kastler E, Viehweger E, Moog R, Amarenco G, Denys P, De Seze M, Haab F, Karsenty G, Kerdraon J, Perrouin-Verbe B, Ruffion A, Soler JM, Saussine C. (2009) Botulinum toxin-A (Botox) intradetrusor injections in children with neurogenic detrusor overactivity/neurogenic overactive bladder: a systematic literature review. Journal of Pediatric Urology. 2009 Jun;5(3):156-64.
Hôpital Rangueil, Toulouse, France. xaviergame@hotmail.com
OBJECTIVES: Describe and discuss the efficacy and safety of botulinum toxin type A (BTX-A) intradetrusor injections in children with neurogenic detrusor overactivity (NDO) and urinary incontinence or overactive bladder symptoms of neurogenic origin (NOAB).
METHODS: A MEDLINE and EMBASE search for clinical studies involving BTX-A injected into the detrusor of children with NDO or NOAB was performed, prior to data analysis.
RESULTS: A total of six articles evaluating the efficacy and safety of Botox in patients with NDO and incontinence/NOAB were selected. The underlying neurological disease was myelomeningocele in 93% of patients. Most were over 2 years of age. The most common amount of Botox injected was 10-12 U/kg with a maximal dose of 300 U, usually as 30 injections of 10 U/ml in the bladder (excluding the trigone) under cystoscopic guidance and general anaesthesia. Most of the studies reported a significant improvement in clinical (65-87% became completely dry) as well as urodynamic (in most studies mean maximum detrusor pressure was reduced to <40 cm H(2)O and compliance was increased >20 ml/cm H(2)O) variables, without major adverse events.
CONCLUSIONS: Botox injections into the detrusor provide a clinically significant improvement and seem to be very well tolerated in children with NDO and incontinence/NOAB refractory to antimuscarinics.
PMID: 19264554
Hôpital Rangueil, Toulouse, France. xaviergame@hotmail.com
OBJECTIVES: Describe and discuss the efficacy and safety of botulinum toxin type A (BTX-A) intradetrusor injections in children with neurogenic detrusor overactivity (NDO) and urinary incontinence or overactive bladder symptoms of neurogenic origin (NOAB).
METHODS: A MEDLINE and EMBASE search for clinical studies involving BTX-A injected into the detrusor of children with NDO or NOAB was performed, prior to data analysis.
RESULTS: A total of six articles evaluating the efficacy and safety of Botox in patients with NDO and incontinence/NOAB were selected. The underlying neurological disease was myelomeningocele in 93% of patients. Most were over 2 years of age. The most common amount of Botox injected was 10-12 U/kg with a maximal dose of 300 U, usually as 30 injections of 10 U/ml in the bladder (excluding the trigone) under cystoscopic guidance and general anaesthesia. Most of the studies reported a significant improvement in clinical (65-87% became completely dry) as well as urodynamic (in most studies mean maximum detrusor pressure was reduced to <40 cm H(2)O and compliance was increased >20 ml/cm H(2)O) variables, without major adverse events.
CONCLUSIONS: Botox injections into the detrusor provide a clinically significant improvement and seem to be very well tolerated in children with NDO and incontinence/NOAB refractory to antimuscarinics.
PMID: 19264554
Tuesday, July 24, 2007
Chiari Type II malformation: past, present, and future.
Stevenson KL. Chiari Type II malformation: past, present, and future. Neurosurgical Focus. 2004 Feb 15;16(2):E5.
OBJECT: The Chiari Type II malformation (CM II) is a unique hindbrain herniation found only in patients with myelomeningocele and is the leading cause of death in these individuals younger than 2 years of age. Several theories exist as to its embryological evolution and recently new theories are emerging as to its treatment and possible prevention. A thorough understanding of the embryology, anatomy, symptomatology, and surgical treatment is necessary to care optimally for children with myelomeningocele and prevent significant morbidity and mortality.
METHODS: A review of the literature was used to summarize the clinically pertinent features of the CM II, with particular attention to pitfalls in diagnosis and surgical treatment.
CONCLUSIONS: Any child with CM II can present as a neurosurgical emergency. Expeditious and knowledgeable evaluation and prompt surgical decompression of the hindbrain can prevent serious morbidity and mortality in the patient with myelomeningocele, especially those younger than 2 years old. Symptomatic CM II in the older child often presents with more subtle findings but rarely in acute crisis. Understanding of CM II continues to change as innovative techniques are applied to this challenging patient population.
PMID: 15209488
OBJECT: The Chiari Type II malformation (CM II) is a unique hindbrain herniation found only in patients with myelomeningocele and is the leading cause of death in these individuals younger than 2 years of age. Several theories exist as to its embryological evolution and recently new theories are emerging as to its treatment and possible prevention. A thorough understanding of the embryology, anatomy, symptomatology, and surgical treatment is necessary to care optimally for children with myelomeningocele and prevent significant morbidity and mortality.
METHODS: A review of the literature was used to summarize the clinically pertinent features of the CM II, with particular attention to pitfalls in diagnosis and surgical treatment.
CONCLUSIONS: Any child with CM II can present as a neurosurgical emergency. Expeditious and knowledgeable evaluation and prompt surgical decompression of the hindbrain can prevent serious morbidity and mortality in the patient with myelomeningocele, especially those younger than 2 years old. Symptomatic CM II in the older child often presents with more subtle findings but rarely in acute crisis. Understanding of CM II continues to change as innovative techniques are applied to this challenging patient population.
PMID: 15209488
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