Aladdin H. Hassanein

Venous malformation: risk of progression during childhood and adolescence.

Venous malformations (VMs) can cause significant morbidity, particularly because they enlarge over time and become symptomatic. The purpose of this study was to determine the natural progression of VMs to facilitate patient counseling, gain insight into pathophysiology, and guide therapy. Our Vascular Anomalies Center database was reviewed for patients with cutaneous and soft-tissue VMs. Predictive variables were age, gender, location, pregnancy, and size. The outcome variable was natural progression of the malformation defined by expansion of the lesion or the onset/worsening of symptoms. The study included 614 patients. Children had a 26.1% risk of progression prior to adolescence, 74.9% before adulthood, and 93.2% over their lifetime. Progression was more likely in adolescence (60.9%) than in childhood (22.5%); the relative risk was 2.6 (95% confidence interval, 2.1–3.2) (P = 0.0001). Diffuse VMs progressed more often than localized lesions (P = 0.002); extremity and trunk VMs worsened more frequently than head/neck lesions (P = 0.03). VMs have a higher risk of progression in adolescents than in children; pubertal hormones may contribute to expansion. Because of their high rate of progression, early treatment of asymptomatic VMs should be considered.

Lymphatic Malformation: Risk of Progression During Childhood and Adolescence

Abstract Lymphatic malformations (LMs) in soft tissues tend to enlarge over time, causing distortion, obstruction, and functional problems. The purpose of this study was to determine the natural progression of LMs to facilitate patient counseling, gain insight into pathophysiology, and guide therapy. Our Vascular Anomalies Center database was reviewed for patients with cutaneous and soft tissue LMs; combined or visceral lesions were excluded. Predictive variables were age, channel type (macrocystic, microcystic, combined), sex, lesion size (localized, diffuse), and location (head/neck, extremities, trunk). The outcome variable was natural progression of the malformation defined by expansion or the onset/worsening of signs and symptoms. The study included 441 patients: 234 females (53.1%) and 207 males (46.9%). Lymphatic malformations were located in the head/neck (61.2%), extremities (17.5%), trunk (16.1%), or multiple sites (5.2%). Children had a 42.2% risk of progression before adolescence, 84.7% before adulthood, and 95.3% during their lifetime. Progression was more likely in adolescence (63.8%) than in childhood (40.8%); the odds ratio was 2.6 (P = 0.003). Diffuse LMs worsened more often than localized lesions (P = 0.001), whereas channel type (P = 0.63), sex (P = 0.42), and location (P = 0.28) did not influence progression. Lymphatic malformations have a greater risk of progression in adolescence than in childhood; pubertal hormones may contribute to expansion. Because of this high rate of progression, early treatment of asymptomatic LMs should be considered.

Expression of androgen, estrogen, progesterone, and growth hormone receptors in vascular malformations.

Background: Vascular malformations frequently enlarge during adolescence, suggesting that hormones may be involved. The purpose of this study was to determine whether pubertal hormone receptors are present in vascular malformations and whether they differ from normal tissue. Methods: Tissue specimens (arteriovenous malformation, lymphatic malformation, and venous malformation) were prospectively collected from patients undergoing resection. Immunohistochemistry was used to determine the presence of androgen, estrogen, progesterone, and growth hormone receptors. The effects of age, sex, location, and malformation type on receptor expression were analyzed. Age-, sex-, and location-matched normal tissues served as controls. Results: Forty-five vascular malformation specimens were collected: arteriovenous malformation (n = 11), lymphatic malformation (n = 20), and venous malformation (n = 14). Growth hormone receptor expression was increased in arteriovenous malformation (72.7 percent), lymphatic malformation (65.0 percent), and venous malformation (57.1 percent) tissues compared with controls (25.8 percent) (p < 0.05). Growth hormone receptor was present primarily in the endothelium/perivasculature of malformations (93.1 percent), whereas in normal tissue growth hormone receptor was located only in the stroma (p < 0.0001). Neither age, nor sex, nor location influenced receptor expression (p = 0.9). No differences in androgen receptor, estrogen receptor, and progesterone receptor staining were found between malformations and control samples (p = 0.7). Conclusions: Growth hormone receptor is overexpressed and principally located in the vessels of vascular malformations. Growth hormone might contribute to the expansion of vascular malformations.

Cranial particulate bone graft ossifies calvarial defects by osteogenesis.

Background: Cranial particulate bone graft heals inlay calvarial defects and can be harvested as early as infancy. The purpose of this study was to test the hypothesis that particulate bone promotes ossification primarily by osteogenesis. Methods: Freshly harvested particulate bone, devitalized particulate bone, and high-speed drilled bone dust from rabbit calvaria were assayed for metabolic activity (resazurin) and viable osteoblasts (alkaline phosphatase). A rabbit cranial defect model was used to test the effect of devitalizing particulate bone on in vivo ossification. A parietal critical-size defect was created and managed in three ways: (1) no implant (n = 6); (2) particulate bone implant (n = 6); and (3) devitalized particulate bone implant (n = 6). Micro–computed tomographic scanning was used to measure ossification 16 weeks later; histology also was studied. Results: Particulate bone contained more viable cells (0.94 percent transmittance per milligram) compared with devitalized particulate bone (0.007 percent) or bone dust (0.21 percent) (p = 0.01). Particulate bone had greater alkaline phosphatase activity (0.13 &mgr;U/&mgr;g) than devitalized particulate bone (0.000) or bone dust (0.06) (p = 0.01). Critical-size defects treated with particulate bone had more ossification (99.7 percent) compared with devitalized particulate bone implants (42.2 percent) (p = 0.01); no difference was found between devitalized particulate bone and the control (40.8 percent) (p = 0.9). Conclusions: Particulate bone graft contains living cells, including osteoblasts, that are required to heal critical-size cranial defects. These data support the hypothesis that particulate bone promotes ossification primarily by osteogenesis.

Management of challenging congenital melanocytic nevi: Outcomes study of serial excision

BACKGROUND Large congenital melanocytic nevi (CMN) cause significant deformity and are at risk for malignant degeneration. Techniques used to remove difficult CMN include serial excision, skin grafting, or tissue expansion. Some authors prefer skin grafting or tissue expansion if several stages would be required to serially resect the CMN. The purpose of this study was to determine the efficacy of serial excision for CMN requiring ≥3 procedures. METHODS Medical records and clinical images of patients with CMN treated between 2007 and 2013 were reviewed. Inclusion criteria were: (1) lesions that required ≥3 serial excisions to remove and (2) CMN that could have been treated reasonably with skin grafting or tissue expansion. Patient age, gender, location of the lesion, size of the CMN, number of serial excisions, and complications were recorded. RESULTS The study included 21 patients. Lesions were located on the lower extremity (38.1%), head/neck (33.3%), upper extremity (14.3%), or trunk (14.3%). Nevus size was 2.2%±1.2% total body surface area. The age during the first operation was 4.3 years (range 3 months to 15 years). The number of excisions was 3.5±0.7, spaced 8.2±4.3 months apart. Partial suture line dehiscence occurred after 2/72 operations and seroma resulted after 1/72 operations; there were no infections. CONCLUSION Challenging CMN amenable to serial excision can be removed effectively and safely using this technique. Children are left with a favorable linear scar, do not have donor or recipient site morbidity from skin grafting, and are not subjected to potential tissue expander complications and injections required for expansion.

Bilateral Upper Extremity Vascular Injury as a Result of a High-Voltage Electrical Burn

High-voltage electrical burns are rare but cause devastating injuries, resulting in potential limb loss and major morbidity and mortality. These injuries are more insidious than flame burns in that the extent of the injury is not obvious at first glance. Damage to underlying muscle, nerve, and vessels may occur, resulting in limb-threatening ischemia and delayed hemorrhage. The management of such injuries remains controversial and can be challenging for the vascular and reconstructive surgeon. We present a case of high-voltage electrical injury to bilateral upper extremities resulting in limb-threatening ischemia, review the literature on the management of such injuries, and propose an algorithm to guide the management of these devastating injuries.

Robot-Assisted Plastic Surgery

Robot assisted surgery is a technology that is being used frequently among multiple surgical specialties; robot assisted microsurgery (RAMS) and transoral robotic surgery (TORS) are applications relevant to plastic surgery that are being studied and clinically utilized. Advantages of RAMS include elimination of tremor and the ability to provide enhanced exposure. TORS facilitates oropharyngeal tumor excision and reconstruction without mandibular splitting. This article investigates current and potential uses of the surgical robot in plastic surgery as well as obstacles to its application.

Reharvested cranial particulate bone graft ossifies inlay calvarial defects.

Abstract Particulate bone graft (PBG) heals calvarial critical-size defects and is procured from the cranium with a hand-driven bit and brace. The donor sites ossify, and thus PBG potentially could be reharvested from the original areas. The purpose of this study was to determine if PBG obtained from a healed donor site is effective for inlay cranioplasty. A 17 × 17-mm critical-size defect was created in the parietal bones of 8 rabbits and treated with either no implant (group 1) or PBG harvested from the frontal bone (group 2). In 4 animals (group 3), a parietal defect was not created initially; PBG was harvested from the frontal bone and then discarded. Sixteen weeks later after the PBG donor sites had healed, a 17 × 17-mm parietal defect was made and filled with PBG reharvested from the previous donor area. Animals underwent micro–computed tomography 16 weeks after inlay cranioplasty. Critical-size defects in controls (group 1) exhibited partial ossification (35.1% ± 10.5%) compared with those treated with PBG (group 2) (99.1% ± 1.5%) or reharvested PBG (group 3) (99.3% ± 1.5%) (P = 0.02). No difference was found between groups 2 and 3 (P = 0.69). Bony thickness was similar in defects implanted with PBG (1.8 mm ± 1.1 mm) or reharvested PBG (2.1 mm ± 0.5 mm) (P = 0.68). Particulate bone graft reharvested from healed donor sites ossifies inlay cranial defects. Because the donor area for PBG is of partial thickness and less than critical size, reparative osteogenesis theoretically allows an unlimited supply of autologous bone for inlay cranioplasty using PBG.

Critical-Size Defect Ossification: Effect of Leporid Age in a Cranioplasty Model

AbstractThe ability of the human cranium to ossify full-thickness defects depends on the size of the area and the age of the patient. An adult leporid cranioplasty model is commonly used to study inlay cranioplasty materials; the influence of age on ossification is unknown in this model. The purpose of this study was to determine the effect of age on healing of a rabbit critical-size defect.Nineteen rabbits were divided into 4 groups: group 1 (n = 5) aged 4 months, group 2 (n = 4) aged 8 months, group 3 (n = 5) aged 12 months, and group 4 (n = 5) aged 16 months. A 17 × 17-mm defect was created in the parietal bones with preservation of the underlying dura. Animals underwent micro–computed tomography 4 months postoperatively to determine ossification of the defect.Group 1 defects healed by 28.5% (SD, 12.5%), group 2 defects ossified by 37.2% (SD, 5.7%), group 3 defects closed by 28.2% (SD, 11.9%), and group 4 defects healed by 39.4% (SD, 11.0%). No difference in ossification was found between groups (P = 0.31).Leporids as young as 4 months do not close a 17 × 17-mm defect; ossification is similar to animals as old as 16 months. Rabbits 4 months or older are suitable for a calvarial critical-size defect model.

Facial infiltrating lipomatosis: expression of angiogenic and vasculogenic factors.

AbstractFacial infiltrating lipomatosis causes diffuse overgrowth of subcutaneous fat, muscle, and bone. Because adipose tissue mass is angiogenesis dependent, the purpose of this study was to determine whether neovascularization is upregulated in this disease.Infiltrating lipomatosis tissue was collected prospectively from the preauricular cheek of 5 patients; neovascularization was compared to normal postauricular adipose. Specimens were analyzed using immunofluorescence for CD31 (microvascular density), &agr;-smooth muscle actin (pericyte marker), CD31/Ki67 (proliferating endothelial cells), and CD34/CD133 (endothelial progenitor cells). Quantitative reverse transcription–polymerase chain reaction was used to determine messenger RNA expression of progenitor cells (CD133) and factors that recruit them: vascular endothelial growth factor (VEGF-A), hypoxia-inducible factor 1&agr;, matrix metalloproteinase 9 (MMP-9), and stromal cell–derived factor 1&agr;. Angiopoietin 1 and 2, MMP-2, VEGF receptors, and neuropilin receptors were quantified using quantitative reverse transcription polymerase chain reaction.There was no difference in microvascular density, pericytic density, or endothelial proliferation between infiltrating lipomatosis and normal adipose tissue (P = 0.2). Expressions of VEGF-A, hypoxia-inducible factor 1&agr;, stromal cell–derived factor 1&agr;, angiopoietin 1 and 2, MMP-2 and -9, VEGF receptors 1 and 2, neuropilin receptors 1 and 2, and CD133 messenger RNA were not elevated compared to control fat (P = 0.1). Endothelial progenitor cells were not present in specimens of infiltrating lipomatosis.Infiltrating lipomatosis does not exhibit elevated angiogenic or vasculogenic factors compared to normal fat; the vasculature is stable. Neovascularization does not seem to play a role in the pathogenesis of this condition.