Six-year Burden of Care for Nonsyndromic Unilateral Cleft Lip and Palate Patients: A Comparison Between Cleft Centers and Noncleft Centers.

OBJECTIVE: To determine differences in burden of care between nonsyndromic patients with unilateral cleft lip and palate undergoing treatment at American Cleft Palate-Craniofacial Association (ACPA)-accredited centers and nonaccredited centers in New York State. DESIGN: A retrospective review of the New York Statewide Planning and Research Cooperative System database from January 2001 to December 2014 was performed using ICD-9 and CPT coding. PATIENTS, PARTICIPANTS: This study included patients with unilateral cleft lip and palate who underwent both lip and palate repairs during their first 6 years of life. Exclusion criteria included orofacial cleft syndromes, follow-up under 6 years, and one-stage combined cleft lip and palate repairs. RESULTS: Eighty-eight patients were treated at cleft centers, and 29 patients at nonaccredited centers ( n = 117). Age at primary palatoplasty (13.0 months vs 18.1 months; p = .019), total number of cleft operations (2.3 vs 2.7; p = .012), and total number of primary cleft-specific procedures (2.2 vs 2.5; p = .0049) were significantly lower for patients treated in cleft centers. Age at primary cheiloplasty (4.8 months vs 4.6 months; p = .865), post-cheiloplasty length of stay (1.2 days vs 1.2 days; p = .673), post-palatoplasty length of stay (1.5 days vs 1.9 days; p = .211), average hospital admissions (2.2 vs 2.3; p = 0.161), and total complication rates (34.1% vs 21.1%; p = 0.517) did not differ significantly between cleft centers and noncenters. CONCLUSIONS: This data demonstrates some significant differences in overall 6 year burden of care for nonsyndromic patients with unilateral cleft lip and palate treated at ACPA-accredited cleft centers versus nonaccredited centers.

Dorsal Fixation of Coronal Hamate and Fifth Metacarpal Base Fractures: An Anatomic Evaluation of the Ulnar Nerve.

PURPOSE: Traumatic drill overshoot during dorsal fixation of coronal hamate and fifth metacarpal base fractures risks iatrogenic ulnar nerve injury. This study describes the anatomic relationships between exiting volar drill tips and ulnar nerve branches. METHODS: Dorsal drilling of hamate bones and fifth metacarpal bases was performed on cadavers. Dorsal hamate bodies were subdivided into 4 quadrants: (1) distal-ulnar, (2) distal-radial, (3) proximal-ulnar, and (4) proximal-radial. Screws measuring 5 mm more than the dorsal-to-volar bone depths were placed in each quadrant to represent drill exit trajectories with consistent overshoot. A single screw was similarly placed 5 mm distal to the midline articular surface of the dorsal fifth metacarpal base. Distances between estimated drill tips and ulnar nerve branches were measured. RESULTS: Ten cadaver hands were examined. The fifth metacarpal base screw tips directly abutted the ulnar motor branch in 6 hands, and were within 1 mm in 4 hands (mean, 0.4 ± 0.5 mm). Distances from the tips to the ulnar motor and sensory branches were largest in the distal-radial quadrant (11.8 ± 0.8 mm and 9.2 ± 1.9 mm, respectively) and smallest in the proximal-ulnar quadrant (7.3 ± 1.5 mm and 4.3 ± 1.1 mm, respectively). Distances to the ulnar motor and sensory branches were similar between the proximal-ulnar and distal-ulnar quadrants, and between the proximal-radial and distal-radial quadrants. CONCLUSIONS: Dorsal drilling of coronal hamate fractures appears to be safe, as volar drill tips are well away from ulnar nerve motor and sensory branches. Distances to ulnar nerve branches are largest, and theoretically safest, with dorsal drilling in the distal-radial hamate. Dorsal drilling of fifth metacarpal base fractures appears to carry a high risk for potential ulnar motor nerve injury. CLINICAL RELEVANCE: These findings may help minimize potential risks for iatrogenic ulnar nerve injury with dorsal drilling of hamate and fifth metacarpal base fractures.

Combined Treatment of High-Flow Scalp Arteriovenous Malformations.

INTRODUCTION: Appropriate treatment of scalp arteriovenous malformations (SAVMs) remains largely unclear given the rarity of reported cases. This single-institution case series presents consecutive patients with extracranial SAVMs and long-term follow up.The primary aim of this study was to review treatment decisions, evaluate clinical outcomes, and compare our experience to available literature in order to better understand SAVMs and improve future outcomes. MATERIALS AND METHODS: A retrospective review of consecutive patients with extracranial SAVMs between January 2015 and December 2019 was performed. Treatment factors of interest included embolization method, embolic agents, and decision to proceed with surgical resection. Relevant clinical outcomes included recurrence rates, cure rates, and complications. RESULTS: Seven patients were included in the present series. Satisfactory outcomes were ultimately achieved for all 7 patients using embolization with or without combined surgical resection. Embolizations performed in combination with resection were curative in 4 of 4 cases (100%). Embolizations performed without resection were curative in 0 of 4 cases (0%), satisfactory in 2 of 4 cases (50%), and unsatisfactory in 2 of 4 cases (50%). DISCUSSION: All SAVM patients in this series were treated satisfactorily using embolization with or without operative resection. This study strongly suggests that embolization combined with surgical resection during the same admission yields the best treatment outcomes for SAVMs, specifically demonstrating lower rates of recurrence and embolization-related complications. Decisions on whether or not to proceed with resection should be made by the interventional radiologist, the plastic surgeon, and the patient together.

Amniotic Band Syndrome: Head-to-Toe Manifestations and Clinical Management Guidelines.

LEARNING OBJECTIVES: After studying this article, the participant should be able to: 1. Understand and describe the basic principles underlying the intrinsic versus extrinsic proposed mechanisms for the development of amniotic band syndrome (ABS). 2. Discuss risk factors and conditions that are associated with the development of ABS. 3. Understand the various presentations and associated clinical implications of ABS by anatomic location. 4. Describe the basic tenets underlying various repair technique options for ABS of the extremities. 5. Discuss the common manifestations of ABS in the face and trunk. 6. Understand clinical implications of fetoscopic surgery as it relates to ABS treatment as a novel method for limb salvage in utero. SUMMARY: Amniotic band syndrome (ABS) refers to the development of constrictive bands of fibrotic tissue in utero. It can lead to a variety of clinical manifestations after delivery. There is much debate in the plastic surgery community regarding the exact pathophysiologic mechanism for the development of ABS, and the most appropriate management. This CME article aims to provide an overview of ABS manifestations throughout the body, and to expound on the most recent advances in anticipatory and definitive management of the condition.

Making the Case for Virtual Surgical Planning: Bilateral Sequential Fibula Flaps with Immediate Dental Implants for Maxillectomy.

SUMMARY: Oncologic maxillectomy defects requiring bony reconstruction are among the most challenging head and neck cases because of the complex three-dimensional geometry of the midface. Virtual surgical planning technology is advantageous in these cases because it provides superior positional precision and accuracy compared with traditional techniques and facilitates prosthodontic rehabilitation. Maxillary cancer recurrence after an initial fibula flap reconstruction presents a unique challenge. The authors report the first two cases of sequential fibula flaps after second or recurrent cancer of the maxilla. Virtual surgical planning facilitated resection with adequate tumor margins, optimized anatomic positioning of the fibula construct with three-dimensional printed plates, and enabled immediate functional dental implant placement.

Low-level blast exposure disrupts gliovascular and neurovascular connections and induces a chronic vascular pathology in rat brain.

Much concern exists over the role of blast-induced traumatic brain injury (TBI) in the chronic cognitive and mental health problems that develop in veterans and active duty military personnel. The brain vasculature is particularly sensitive to blast injury. The aim of this study was to characterize the evolving molecular and histologic alterations in the neurovascular unit induced by three repetitive low-energy blast exposures (3 × 74.5 kPa) in a rat model mimicking human mild TBI or subclinical blast exposure. High-resolution two-dimensional differential gel electrophoresis (2D-DIGE) and matrix-assisted laser desorption/ionization (MALDI) mass spectrometry of purified brain vascular fractions from blast-exposed animals 6 weeks post-exposure showed decreased levels of vascular-associated glial fibrillary acidic protein (GFAP) and several neuronal intermediate filament proteins (α-internexin and the low, middle, and high molecular weight neurofilament subunits). Loss of these proteins suggested that blast exposure disrupts gliovascular and neurovascular interactions. Electron microscopy confirmed blast-induced effects on perivascular astrocytes including swelling and degeneration of astrocytic endfeet in the brain cortical vasculature. Because the astrocyte is a major sensor of neuronal activity and regulator of cerebral blood flow, structural disruption of gliovascular integrity within the neurovascular unit should impair cerebral autoregulation. Disrupted neurovascular connections to pial and parenchymal blood vessels might also affect brain circulation. Blast exposures also induced structural and functional alterations in the arterial smooth muscle layer. Interestingly, by 8 months after blast exposure, GFAP and neuronal intermediate filament expression had recovered to control levels in isolated brain vascular fractions. However, despite this recovery, a widespread vascular pathology was still apparent at 10 months after blast exposure histologically and on micro-computed tomography scanning. Thus, low-level blast exposure disrupts gliovascular and neurovascular connections while inducing a chronic vascular pathology.

Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI.

Blast-related traumatic brain injury (TBI) has been a common cause of injury in the recent conflicts in Iraq and Afghanistan. Blast waves can damage blood vessels, neurons, and glial cells within the brain. Acutely, depending on the blast energy, blast wave duration, and number of exposures, blast waves disrupt the blood-brain barrier, triggering microglial activation and neuroinflammation. Recently, there has been much interest in the role that ongoing neuroinflammation may play in the chronic effects of TBI. Here, we investigated whether chronic neuroinflammation is present in a rat model of repetitive low-energy blast exposure. Six weeks after three 74.5-kPa blast exposures, and in the absence of hemorrhage, no significant alteration in the level of microglia activation was found. At 6 weeks after blast exposure, plasma levels of fractalkine, interleukin-1ß, lipopolysaccharide-inducible CXC chemokine, macrophage inflammatory protein 1α, and vascular endothelial growth factor were decreased. However, no differences in cytokine levels were detected between blast-exposed and control rats at 40 weeks. In brain, isolated changes were seen in levels of selected cytokines at 6 weeks following blast exposure, but none of these changes was found in both hemispheres or at 40 weeks after blast exposure. Notably, one animal with a focal hemorrhagic tear showed chronic microglial activation around the lesion 16 weeks post-blast exposure. These findings suggest that focal hemorrhage can trigger chronic focal neuroinflammation following blast-induced TBI, but that in the absence of hemorrhage, chronic neuroinflammation is not a general feature of low-level blast injury.

Selective vulnerability of the cerebral vasculature to blast injury in a rat model of mild traumatic brain injury.

BACKGROUND: Blast-related traumatic brain injury (TBI) is a common cause of injury in the military operations in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. The aim of the present study was to examine whether blast exposure affects the cerebral vasculature in a rodent model. We analyzed the brains of rats exposed to single or multiple (three) 74.5 kPa blast exposures, conditions that mimic a mild TBI. Rats were sacrificed 24 hours or between 6 and 10 months after exposure. Blast-induced cerebral vascular pathology was examined by a combination of light microscopy, immunohistochemistry, and electron microscopy. RESULTS: We describe a selective vascular pathology that is present acutely at 24 hours after injury. The vascular pathology is found at the margins of focal shear-related injuries that, as we previously showed, typically follow the patterns of penetrating cortical vessels. However, changes in the microvasculature extend beyond the margins of such lesions. Electron microscopy revealed that microvascular pathology is found in regions of the brain with an otherwise normal neuropil. This initial injury leads to chronic changes in the microvasculature that are still evident many months after the initial blast exposure. CONCLUSIONS: These studies suggest that vascular pathology may be a central mechanism in the induction of chronic blast-related injury.