Correspondence and communications

Figure 2

429

Evidence-based protocol for the management of dog bites. Figure revised from Morgan et al. and Evgeniou et al.1,2

A guideline for the management of dog bites across the UK would make treatment of dog bites more consistent and our overall management approach more effective. The following is a recommended protocol on the management of dog bites based on the evidence in the literature (Figure 2).

Funding No funding was provided for this article.

5. Holm M, Tarnvik H. Hospitalisation due to Pasteurella multocidadinfected animal bite wounds: correlation with inadequate primary antibiotic medication. Scand J Infect Dis 2000; 32:181e3.

Sarah Al-Himdani Kian T. Tan Christopher G. Duff Department of Plastic and Reconstructive Surgery, University Hospital of South Manchester NHS Foundation Trust, M23 9LT, UK E-mail address: [email protected]

Conflict of interest None declared.

ª 2014 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.

Ethical approval

http://dx.doi.org/10.1016/j.bjps.2014.10.025

N/A.

References 1. Morgan M, Palmer J. Dog bites. BMJ 2007;334:413e7. 2. Evgeniou E, Markeson D, Iyer S, Armstrong A. The management of animal bites in the United Kingdom. Eplasty 2013;13:e27. 3. Dire DJ, Hogan DE, Walker JS. Prophylactic oral antibiotics for low-risk dog bite wounds. Pediatr Emerg Care 1992;8(4):194e9. 4. National Institute for Health and Care Excellence (NICE). Biteshuman and animal. 2012. Available from: http://cks.nice.org. uk/bites-human-and-animal [accessed 05.08.14].

Response to “Seat belt injury causing bisection of the breast: A case report” Dear Sir, I read with interest the article “Seat belt injury causing bisection of the breast: A case report” by Teo et al.1

430 The authors describe a pattern of injury, namely breast bisection, caused by the diagonal component of a seat-belt restraint due the rapid deceleration and subsequent compression caused when the locking mechanism engages during vehicular collision. Despite some US physicians equipping their own cars with lap belts since the 1930s and car manufacturers including Volvo, Ford and Chrysler offering lap belts in their cars in 1956, it only became compulsory for car manufacturers to provide lap belts in 1964. Irrespective of this, various Bills concerning the compulsory wearing of seat belts proposed during the 1970s were either shelved or defeated until Lord Nugent’s (RoSPA’s president) successful campaign in 1981. The Bill became law and as the authors state, it first became compulsory for drivers and passengers to wear seat belts in 1983. A study published by the Transport and Road Research Laboratories in 1985 confirmed that the new law had increased seat belt usage from 40% to 95% amongst drivers and front seat passengers and that this was associated with a 25% reduction in driver fatality and 29% reduction in front seat passenger fatality.2 It is generally accepted that the injuries caused by the modern 3-point belt (first patented in 1958) are acceptable consequences of this life-saving design, which is recognised to reduce the impact of a passenger to about a fifth of the impact suffered by the body of the car. Even so, in an accident model involving a 70 kg driver and a car stopping distance of 1 foot from a speed of 30 mph, the force on the driver is approximately 2.4tons.3 As highlighted in the published article, one mechanism of seat-belt injury is a closed linear compression force diagonally traversing the breast (commensurate with the position and direction of the belt), the extent of which may go unrecognised at initial presentation. Resulting fat necrosis causes a cleft in the underlying breast tissue and resorption of volume leading to breast asymmetry. We have recently treated a similar patient; a 69 year-old front seat passenger involved in an RTA in Germany. Our patient presented 4 months following the accident with a similar pattern of injury. In addition to the fat necrosis and cleft, it should be noted that if that cleft traverses the breast meridian, the subsequent scarring tethers the nipple areolar complex (NAC) to the chest wall, as further eluded to in the report by Paddle et al.,4 (referenced by the authors). Furthermore, it is possible that the cleft is associated with a seroma cavity, having further implications for reconstruction. Consistent with the reported case, we found that the volume of the injured breast was significantly reduced resulting in obvious breast asymmetry (Figure 1). In their case, Teo and colleagues describe incising the edges of the cleft, maintaining nipple-areolar perfusion on a predetermined vascular pedicle (in their case a superolateral pedicle), and re-approximation of the breast pillars. In our case the edges of the cleft were excised but a modification from the published report includes limiting this incision from the inferior limit of the cleft to a point on the upper border of the NAC in order to avoid placing a scar in the cleavage area of the breast. Furthermore, the underlying seroma cavity was excised and the breast pillars closed using a layered closure to further correct the cleft. NAC vascularity was maintained on a broad superior pedicle

Correspondence and communications

Figure 1

Pre-operative view.

and the NAC was repositioned on a de-epithelialised dermal base on the opposing breast pillar. A slight residual depression in the upper medial quadrant of the breast was treated with liposculpture and the patient is due to

Figure 2

Post-operative view.

Correspondence and communications undergo contralateral symmetrising reduction mammaplasty (Figure 2). Based on limited reports in the literature, we conclude that this pattern of injury is associated with the triad of fat necrosis, clefting of the breast and associated tethering of skin (which may result in distortion of the NAC). Reconstruction is simple and involves excision of the cleft (þ/ seroma cavity), repositioning of the NAC and symmetrisation of the contralateral breast if necessary. Scarring on the visible cleavage area and residual defects in the upper pole can be minimised by the concomitant use of liposculpture.

Conflict of interest N/A.

Funding N/A.

Ethical approval N/A.

References 1. Teo I, Dujon D, Azmy I. Seat belt injury causing bisection of the breast: a case report. J Plastic Reconstr Aesthetic Surg JPRAS 2014;67(7):1008e9. 2. Scott PP, W. P. TRRL research report. 1985. p. 985. 3. Available from: hyperphysics.phy-astr.gsu.edu. 4. Paddle AM, Morrison WA. Seat belt injury to the female breast: review and discussion of its surgical management. ANZ J Surg 2010;80(1e2):71e4.

N.C. Petrie Consultant Plastic and Reconstructive Surgeon, Department of Plastic and Reconstructive Surgery, John Radcliffe Hospital, Oxford, UK DOI of original article: http://dx.doi.org/10.1016/j.bjps.2014. 01.024 ª 2014 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.bjps.2014.10.026

Rib osteomyelitis: An uncommon complication of breast implant infection Dear Sir, Rib osteomyelitis (RO) is a disease that is rarely reported.1 The purpose of this paper is to report on the first 3 cases of RO as a complication of breast implant infection (BII)

431 recorded in a cohort study of 37 cases of BI managed from January 2008 to June 2012 in an inter-regional referral center for bone/joint infections in the south of France. Our center is also a regional referral center for plastic/reconstructive surgery that managed 1350 breast implant (BI) included 217 definitive implants for reconstruction (DIR) and 1133 esthetic breast augmentations (EBA) during the study period. - 1st case: A 77-year-old woman was admitted for breast implant exchange nine years after EBA. The BI type was poly implant prostheses (PIP). After surgical resection, a peripherally located cutaneous siliconoma in the right breast was confirmed on histology. The patient presented a swelling, reddish and painful right breast 2 months after surgery. She also had a fistula until the 4th right rib, with purulent discharge and without fever. Deep-sample and bone biopsy cultures were positive for Staphylococcus aureus. She was treated with surgical debridement and discharged after 3 months of association of rifampicin and ofloxacin. - 2nd case: A 41-year-old woman underwent a mastectomy and radiotherapy for breast cancer. She had received BI for DIR. The patient had no other predisposing factor for infection. The postoperative evolution was characterized by intermittent local inflammation, resolved by short courses of antibiotic treatment. A perioperative diagnosis of RO related to BII by S. aureus was performed. The patient was discharged after prosthesis removal combined with surgical debridement and 3 months of association of rifampicin and ofloxacin. - 3rd case: A 60-year-old woman had received BI for EBA. She presented purulent discharge from the scar 2 weeks after the surgery. She was treated with repeated short courses of antibiotic treatment with amoxicillin and clavulanic acid for several months. A diagnosis of RO and BII was made during surgical breast implant removal. Deep samples and bone biopsies were positive for S. aureus and Pseudomonas aeruginosa. The patient was discharged after surgical debridement and 3 months of association of ceftazidime, ciprofloxacin and rifampicin. We herein report 3 cases of RO related to BII over 4.5 years of experience. For these patients, BI were made by experienced breast surgeons of private clinics in the region. We have supported these cases as inter-regional referral center for plastic/reconstructive surgery. In two of the cases of EBA, BI were inserted in the retro-muscular space at the level of the periosteum through inframammary fold. In one case, BI had been placed for DIR. Silicone implants were used in the 3 cases. RO is uncommon and usually occurs in patients with predisposing factors i.e. pneumonia, lung empyema, chest trauma, chronic granulomatous disease, neutropenia, sickle-cell disease, thalassemia or disseminated infections.1,2 Three cases of RO related to BII were caused by S. aureus and 1 case caused by P. aeruginosa. These bacteria were known as classical microorganism involved in chronic osteitis and BII.1,3e5 Among the 3 cases of chronic RO related to BII, the median age of the patients was 60 years (18 years, range 41e77). The mean time to the diagnosis of chronic RO after

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