Central Coalition Osteotomy of Phalangeal Synostoses in the Management of the Type III Apert Hand.

PURPOSE: We report a technique in the management of the type III Apert hand. The proposed approach facilitates the creation of a 5-fingered hand in 3 stages. METHODS: We reviewed records of patients with Apert syndrome and type III hands surgically treated at our institution from 1995 through 2014. In all cases, syndactyly release was performed in 3 stages with prioritization of the border digits. In addition, limited retrograde, axial osteotomies between the phalangeal segments of the conjoined index, middle, and ring fingers were performed during the first stage. Medical records were reviewed for demographics, clinical presentation, operative findings, and postoperative outcomes. RESULTS: Twelve pediatric patients with type III hands underwent syndactyly release. Median patient age was 10.0, 15.8, and 29.6 months at operative stages 1, 2, and 3, respectively. A thumb and 4 fingers were achieved for all but 1 hand. The median duration of hospital stay was 2 days for each stage. No infections or major complications were observed. CONCLUSIONS: We demonstrate this method as a safe and effective means of creating 5 digits in the Apert patient with type III hands. Our opinion is that the additional aesthetic and functional gains offset the requirement of a 3-stage approach. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic IV.

Is There Bias against Simulation in Microsurgery Training?

Background While other surgical specialties have embraced virtual reality simulation for training and recertification, microsurgery has lagged. This study aims to assess the opinions of microsurgeons on the role of simulation in microsurgery assessment and training. Methods We surveyed faculty members of the American Society of Reconstructive Microsurgery to ascertain opinions on their use of simulation in training and opinions about the utility of simulation for skills acquisition, teaching, and skills assessment. The 21-question survey was disseminated online to 675 members. Results Eighty-nine members completed the survey for a 13.2% response rate. Few microsurgeons have experience with high-fidelity simulation, and opinions on its utility are internally inconsistent. Although 84% of respondents could not identify a reason why simulation would not be useful, only 24% believed simulation is a useful measure of clinical performance. Nearly three-fourths of respondents were skeptical that simulation would improve their skills. Ninety-four percent had no experience with simulator-based assessment. Conclusion Simulation has been shown to improve skills acquisition in microsurgery, but our survey suggests that unfamiliarity may foster bias against the technology. Failure to incorporate simulation may adversely affect training and may put surgeons at a disadvantage should these technologies be adopted for recertification by regulatory agencies.

Discrepancies between meeting abstracts and subsequent full text publications in hand surgery.

PURPOSE: Research abstracts presented during the proceedings of an annual meeting are often cited and can influence clinical practice. Prior studies show that roughly 50% of abstracts at American Society for Surgery of the Hand meetings are eventually published. Yet, it is unknown how often the results or conclusions of published studies differ from the podium presentation. The objective of this study was to quantify the differences between abstracts presented during the annual meeting of the American Society for Surgery of the Hand and the resulting manuscripts. METHODS: We retrospectively reviewed every abstract delivered as a podium presentation at the American Society for Surgery of the Hand annual meeting from 2000 to 2010. We searched the PubMed database for matching publications and compared authorship, country of origin, hypothesis, study design and methodology, changes in study groups or populations, results, and conclusions. RESULTS: Of 798 total abstracts, we analyzed 719 involving the hand, wrist, and brachial plexus. Fifty-six different journals published 393 of the abstracts, for a 49% publication rate. Mean time to publication was 18 months with a median of 14 and maximum of 122 months. There were inconsistencies between the results and/or conclusions in 14% of full-length articles compared with the abstract presented at the meeting. A total of 9% of articles were published with fewer subjects. Authorships changes were noted in 54% of publications. CONCLUSIONS: Abstracts represent preliminary investigations and major and minor changes occur before subsequent publication. Caution should be exercised in referencing abstracts or altering clinical practice based on their content. TYPE OF STUDY/LEVEL OF EVIDENCE: Economic/decision analysis IV.

Upper extremity anomalies in Pfeiffer syndrome and mutational correlations.

BACKGROUND: Pfeiffer syndrome is characterized by craniosynostosis and a variety of associated upper and lower extremity anomalies. The authors reviewed presentation and treatment of upper extremity anomalies in a series of genotyped patients with Pfeiffer syndrome. METHODS: Medical records of patients with Pfeiffer syndrome seen at the authors' institution over a 16-year period were reviewed. Data on clinical presentation, genetic testing, and treatment were collected. The upper extremity anomalies were documented using plain radiographs and physical examinations by a multidisciplinary craniofacial team. RESULTS: Of 15 patients identified as having FGFR1- or FGFR2-confirmed Pfeiffer syndrome, 12 (80 percent) presented with upper extremity anomalies, most commonly broad thumbs [n = 10 (83 percent)], radial clinodactyly (thumbs) [n = 7 (58 percent)], and symphalangism [n = 7 each (58 percent)]. All patients with upper extremity anomalies had lower extremity anomalies. Six of the 12 patients (50 percent) with upper extremity findings underwent surgical correction. FGFR1 or FGFR2 genotype did not correlate with upper extremity phenotype. CONCLUSIONS: Although broad thumbs are common, patients with Pfeiffer syndrome often present with other upper extremity anomalies that may not require surgical intervention. Genetic and allelic heterogeneity may explain phenotypic variability in these upper extremity anomalies. Characterization of these limb differences should be made by pediatric hand surgeons as part of a craniofacial team. Treatment decisions should be individualized and dictated by the type and severity of clinical presentation. CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, IV.

Why we are here: early reflections on the role of reconstructive plastic surgery in the 2013 Boston marathon bombings.

The 2013 Boston Marathon bombings resulted in a large and unexpected influx of patients requiring acute multidisciplinary surgical care. The authors describe the surgical management experience of these patients at Brigham & Women's Hospital and Brigham & Women's Faulkner Hospital, with a particular focus on the important role played by reconstructive plastic surgery. The authors suggest that this experience illustrates the value of reconstructive plastic surgery in the treatment of these patients specifically and of trauma patients in general, and argue for the increasing importance of promoting our identity as a specialty.

Nonoperative management of patients with a diagnosis of high-grade small bowel obstruction by computed tomography.

OBJECTIVE: To determine the natural history and treatment of high-grade small bowel obstruction (HGSBO). Small bowel obstruction is a frequent complication of abdominal surgery. Complete and strangulating obstructions are managed operatively while partial obstructions receive a trial of nonoperative therapy. The management and outcome of patients with HGSBO diagnosed by computed tomography (CT) has not been examined. DESIGN: Retrospective medical record review. Outcomes for nonoperative vs operative management were analyzed using Fisher exact and log-rank tests. SETTING: Tertiary care referral center. PATIENTS: One thousand five hundred sixty-eight consecutive patients admitted from the emergency department with a diagnosis of small bowel obstruction between 2000 and 2005 by CT criteria. MAIN OUTCOME MEASURES: Recurrence of symptoms and complications. RESULTS: One hundred forty-five patients (9%) with HGSBO were identified, with 88% follow-up (median, 332 days; range, 4-2067 days). Sixty-six (46%) were successfully managed nonoperatively while 79 (54%) required an operation. Length of stay and complications were significantly increased in the operative group (4.7 days vs 10.8 days and 3% vs 23%; P < .001). Nonoperative management was associated with a higher recurrence rate (24% vs 9%; P < .005) and shorter time to recurrence (39 days vs 105 days; P < .005) compared with operative intervention. Computed tomography signs of ischemia, admission laboratory results, and presence of cancer or inflammatory bowel disease were not predictive of an operation. CONCLUSIONS: Patients with HGSBO by CT can be managed safely with nonoperative therapy; however, they have a significantly higher rate of recurrence requiring readmission or operation within 5 years.

PTH(1-34) replacement therapy in a child with hypoparathyroidism caused by a sporadic calcium receptor mutation.

Autosomal dominant hypocalcemia (ADH) is an inherited form of hypoparathyroidism caused by activating mutations in the calcium-sensing receptor (CaR). Treatment with PTH(1-34) may be superior to conventional therapy but is contraindicated in children, and long-term effects on the skeleton are unknown. The patient is a 20-yr-old female with ADH treated with PTH continuously since 6 yr and 2 mo of age. A bone biopsy was obtained for histomorphometry and quantitative backscattered electron imaging (qBEI). Her data were compared with one age-, sex-, and length of hypoparathyroidism-matched control not on PTH and two sex-matched ADH controls before and after 1 yr of PTH. The patient's growth was normal. Hypercalciuria and hypermagnesuria persisted despite normal or subnormal serum calcium and magnesium levels. Nephrocalcinosis, without evidence of impaired renal function, developed by 19 yr of age. Cancellous bone volume was dramatically elevated in the patient and in ADH controls after 1 yr of PTH. BMD distribution (BMDD) by qBEI of the patient and ADH controls was strikingly shifted toward lower mineralization compared with the non-ADH control. Moreover, the ADH controls exhibited a further reduction in mineralization after 1 yr of PTH. These findings imply a role for CaR in bone matrix mineralization. There were no fractures or osteosarcoma. In conclusion, long-term PTH replacement in a child with ADH was not unsafe, increased bone mass without negatively impacting mineralization, and improved serum mineral control but did not prevent nephrocalcinosis. Additionally, this may be the first evidence of a role for CaR in human bone.

Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation.

We previously reported that genetically obese mice exhibit innate airway hyperresponsiveness (AHR) and enhanced ozone (O(3))-induced pulmonary inflammation. Such genetic deficiencies in mice are rare in humans, and they may not be representative of human obesity. Thus the purpose of this study was to determine the pulmonary phenotype of mice with diet-induced obesity (DIO), which more closely mimics the cause of human obesity. Therefore, wild-type C57BL/6 mice were reared from the time of weaning until at least 30 wk of age on diets in which either 10 or 60% of the calories are derived from fat in the form of lard. Body mass was approximately 40% greater in mice fed 60 vs. 10% fat diets. Baseline airway responsiveness to intravenous methacholine, measured by forced oscillation, was greater in mice fed 60 vs. 10% fat diets. We also examined lung permeability and inflammation after exposure to room air or O(3) (2 parts/million for 3 h), an asthma trigger. Four hours after the exposure ended, O(3)-induced increases in bronchoalveolar lavage fluid protein, interleukin-6, KC, macrophage inflammatory protein-2, interferon-gamma-inducible protein-10, and eotaxin were greater in mice fed 60 vs. 10% fat diets. Innate AHR and augmented responses to O(3) were not observed in mice raised from weaning until 20-22 wk of age on a 60% fat diet. These results indicate that mice with DIO exhibit innate AHR and enhanced O(3)-induced pulmonary inflammation, similar to genetically obese mice. However, mice with DIO must remain obese for an extended period of time before this pulmonary phenotype is observed.

Allergic airway responses in obese mice.

RATIONALE: Epidemiologic data indicate an increased incidence of asthma in the obese. OBJECTIVES: To determine whether obese mice exhibit augmented pulmonary responses after allergen sensitization and challenge. METHODS: Lean, wild-type (C57BL/6), obese ob/ob, and obese db/db mice were sensitized to ovalbumin (OVA), and then challenged with aerosolized OVA or phosphate-buffered saline (PBS). Changes in total pulmonary resistance (Rl) induced by intravenous methacholine were measured by forced oscillation. Blood was collected, bronchoalveolar lavage (BAL) was performed, and lungs were harvested for measurement of cytokine expression by real-time reverse transcription-polymerase chain reaction. MEASUREMENTS AND MAIN RESULTS: OVA challenge increased baseline Rl in ob/ob, but not wild-type, mice, and airway responsiveness was greater in ob/ob than wild-type mice, regardless of the challenge. Compared with PBS, OVA challenge caused an increase in the number of BAL fluid (BALF) cells, an increase in lung Th2 cytokine expression, and an increase in serum IgE. Significantly fewer BALF cells were recovered from OVA-challenged ob/ob versus wild-type mice, whereas serum IgE levels were elevated significantly more in ob/ob versus wild-type mice. BALF and lung Th2 cytokine expression was not different in ob/ob versus wild-type mice. Airway responsiveness was greater in db/db versus wild-type mice, regardless of the challenge, and OVA caused airway hyperresponsiveness in db/db but not wild-type mice, despite reduced BALF cells in OVA-challenged db/db versus wild-type mice. CONCLUSIONS: These results demonstrate that obesity enhances OVA-induced changes in pulmonary resistance and serum IgE and that these changes are not the result of increased Th2 type airway inflammation.

Pulmonary responses to acute ozone exposure in fasted mice: effect of leptin administration.

Leptin is a satiety hormone that also has proinflammatory effects, including augmentation of ozone-induced pulmonary inflammation. The purpose of this study was to determine whether reductions in endogenous levels of leptin can attenuate pulmonary responses to ozone. To reduce serum leptin, we fasted mice overnight before ozone exposure. Fasting caused a marked reduction in serum leptin to approximately one-sixth the levels observed in fed mice, and continuous infusion of leptin via Alzet micro-osmotic pumps restored serum leptin to, but not above, fed levels. Ozone exposure (2 ppm for 3 h) caused a significant, approximately 40% increase in pulmonary resistance (P < 0.01) and increased airway responsiveness in fasted but not in fed mice. The increased effect of ozone on pulmonary mechanics and airway responsiveness in fasted mice was not observed when leptin was restored via continuous infusion. Ozone exposure caused pulmonary inflammation, as evident by increases in bronchoalveolar lavage cells, protein, and soluble tumor necrosis factor receptors. There was no effect of fasting status on ozone-induced changes in the bronchoalveolar lavage inflammatory profile, and leptin treatment did not alter these responses. Our results indicate that fasting augments ozone-induced changes in pulmonary mechanics and airway responsiveness in mice. These effects of fasting are the result of declines in serum leptin. The mechanistic basis for this protective effect of leptin in fasted mice remains to be determined but is not related to effects on ozone-induced inflammation.

Augmented responses to ozone in obese carboxypeptidase E-deficient mice.

We reported previously that mice obese as a result of leptin deficiency (ob/ob) have enhanced ozone (O3)-induced airway hyperresponsiveness (AHR) and inflammation compared with wild-type (C57BL/6) controls. To determine whether this increased response to O3 was independent of the modality of obesity, we examined O3-induced AHR and inflammation in Cpe(fat) mice. These mice are obese as a consequence of a mutation in the gene encoding carboxypeptidase E (Cpe), an enzyme important in processing prohormones and proneuropeptides involved in satiety and energy expenditure. Airway responsiveness to intravenous methacholine, measured by forced oscillation, was increased in Cpe(fat) vs. wild-type mice after air exposure. In addition, compared with air exposure, airway responsiveness was increased 24 h after O3 exposure (2 ppm for 3 h) in Cpe(fat) but not in wild-type mice. Compared with air-exposed controls, O3 exposure increased bronchoalveolar lavage fluid (BALF) protein, IL-6, KC, MIP-2, MCP-1, and soluble TNF receptors (sTNFR1 and sTNFR2) as well as BALF neutrophils. With the exception of sTNFR1 and sTNFR2, all of these outcome indicators were greater in Cpe(fat) vs. wild-type mice. Serum sTNFR1, sTNFR2, MCP-1, leptin, and blood leukocytes were elevated in Cpe(fat) compared with wild-type mice even in the absence of O3 exposure, similar to the chronic systemic inflammation observed in human obesity. These results indicate that increased O3-induced AHR and inflammation are consistent features of obese mice, regardless of the modality of obesity. These results also suggest that chronic systemic inflammation may enhance airway responses to O3 in obese mice.

Increased pulmonary responses to acute ozone exposure in obese db/db mice.

Epidemiological studies indicate the incidence of asthma is increased in obese and overweight humans. Responses to ozone (O(3)), an asthma trigger, are increased in obese (ob/ob) mice lacking the satiety hormone leptin. The long form of leptin receptor (Ob-R(b)) is required for satiety; mice lacking this receptor (db/db mice) are also substantially obese. Here, wild-type (WT) and db/db mice were exposed to air or O(3) (2 ppm) for 3 h. Airway responsiveness, measured by the forced oscillation technique, was greater in db/db than WT mice after air exposure. O(3)-induced increases in pulmonary resistance and airway responsiveness were also greater in db/db mice. BALF eotaxin, IL-6, KC, and MIP-2 increased 4 h after O(3) exposure and subsided by 24 h, whereas protein and neutrophils continued to increase through 24 h. For each outcome, the effect of O(3) was significantly greater in db/db than WT mice. Previously published results obtained in ob/ob mice were similar except for O(3)-induced neutrophils and MIP-2, which were not different from WT mice. O(3) also induced pulmonary IL-1beta and TNF-alpha mRNA expression in db/db but not ob/ob mice. Leptin was increased in serum of db/db mice, and pulmonary mRNA expression of short form of leptin receptor (Ob-R(a)) was similar in db/db and WT mice. These data confirm obese mice have innate airway hyperresponsiveness and increased pulmonary responses to O(3). Differences between ob/ob mice, which lack leptin, and db/db mice, which lack Ob-R(b) but not Ob-R(a), suggest leptin, acting through Ob-R(a), can modify some pulmonary responses to O(3).