Images for surgeons
malities at chromosomal region 8q11-13, while a distinctive translocation t(12;16) (q13;p11) is observed with myxoid liposarcomas.8 In contrast, liposarcomas are rare before the age of 5 years, which virtually excludes it from the differential diagnosis of a neck lump in infancy and early childhood.1 Imaging is not useful in differentiating the two. On computed tomography imaging, the lesion appears radioopaque and non-enhancing with the same Hounsfield density as fat. On MRI, the lesion usually appears lobulated and heterogenous with streaks and whorls and is able to be differentiated from subcutaneous fat on T1- and T2-weighted images because of the presence of immature lipoblasts. Unlike subcutaneous fat, lipoblastomas demonstrate high signal intensity on fat suppression, making this a potential diagnostic characteristic.9
References Fig. 2. Intraoperative photo of the tumour, which was completely excised with preservation of the accessory nerve.
presenting in the first year of life.2 Twice as many men as women are affected.3 Surgical excision is usually curative, however recurrence rates of between 14% and 24% have been reported.3,4 Other head and neck tumours encountered for a child this age include neuroblastoma, rhabdomyosarcoma, lymphoma and nonrhabdomyosarcoma soft tissue sarcomas.5 In the older literature, the terms lipoblastoma, lipoblastomatosis and hibernoma have been used interchangeably, leading to some confusion. At present, the term lipoblastoma is used to refer to the well-encapsulated variety containing more myxoid stroma with peripheral infiltration and distribution throughout all the tissue layers. Lipoblastomatosis currently refers to the more diffuse and infiltrative tumour type, which is distributed in the deep layer and is more likely to recur after surgery.6 Hibernomas are gray-brown, lobulated tumours arising from brown fat.7 Histologically, lipoblastomas contain immature fat cells in varying stages of maturity with septae between the cells dividing them into lobules. These are differentiated from myxoid liposarcomas, the most common histological type among children, by observing poorly defined lobulation with larger lobules, atypical nuclei, abnormal mitoses and the presence of mucinous pools.3 Liposarcomas may resemble lipoblastomas histologically, making diagnosis difficult. Chromosomal analysis might help to differentiate the two. Lipoblastomas are associated with breakpoint abnor-
1. Collins MH, Chatten J. Lipoblastoma/lipoblastomatosis: a clinicopathologic study of 25 tumors. Am. J. Surg. Pathol. 1997; 21: 1131–7. 2. Coffin CM. Lipoblastoma: an embryonal tumor of soft tissue related to organogenesis. Semin. Diagn. Pathol. 1994; 11: 98–103. 3. Pham NS, Poirier B, Fuller SC. Pediatric lipoblastoma in the head and neck: a systematic review of 48 reported cases. Int. J. Pediatr. Otorhinolaryngol. 2010; 74: 723–8. 4. Hicks J, Dilley A, Patal D et al. Lipoblastoma and lipoblastomatosis in infancy and childhood: histopathologic, ultrastructural, and cytogenetic features. Ultrastruct. Pathol. 2001; 25: 321–33. 5. Flint PW, Haughey BH, Lund VJ, Niparko JK. Cummings Otolaryngology: Head & Neck Surgery, 5th edn. Maryland Heights, MO: Mosby Elsevier, 2010; Ch. 200. 6. Chung EB, Enzinger FM. Benign lipoblastomatosis. An analysis of 35 cases. Cancer 1973; 32: 482–92. 7. Greco MA, Garcia RL, Vuletin JC. Benign lipoblastomatosis: ultrastructure and histogenesis. Cancer 1980; 45: 511–5. 8. Chen Z, Coffin CM, Scott S et al. Evidence by spectral karyotyping that 8q11.2 is nonrandomly involved in lipoblastoma. J. Mol. Diagn. 2000; 2: 73–7. 9. Rosen A, Jedynak AR, Respler D. Lipoblastoma of the neck mimicking cystic hygroma. Otolaryngol. Head Neck Surg. 2005; 132: 511–3.
Rebecca Sin Mei Lim, MBBS (Hons) Sam Flatman, MBBS, BSc Elizabeth Sigston, MBBS, FRACS Anthony Longano, MD Ear, Nose and Throat Department, Southern Health, Melbourne, Victoria, Australia doi: 10.1111/ans.12238
Millipede burn masquerading as trash foot in a paediatric patient A 14-year-old female presented to the emergency department of a regional hospital with apparent full thickness necrosis of the medial right three toes and scattered dark patches on the heel and lateral aspect of that foot (Fig. 1). The patient had no previous medical history of note and did not take any regular medications. Additionally, she had no remarkable familial
history of autoimmune or vasculitic disease. On admission, the patient was afebrile, haemodynamically stable and appeared systemically well. Examination of her peripheries revealed a number of well-circumscribed dark patches on the distal aspects of her right first, second and third toes, as well as patchy dark lesions on the lateral foot and heel, consistent with a clinical picture of trash foot with localized © 2013 Royal Australasian College of Surgeons
Images for surgeons
Fig. 1. Appearance of trash foot on admission.
Fig. 2. Apparent necrosis of first three toes.
necrosis (Fig. 2). However, on further examination, the foot was warm and non-tender to palpation. Robust pedal pulses were detected bilaterally, and a full cardiovascular examination was unremarkable. The patient was admitted for further investigation. Full blood count, autoimmune and vasculitis screens were all normal. Inflammatory markers were all within normal limits. Transthoracic echography revealed no valvular abnormality or cardiac thrombus. The vascular surgery service was consulted for an opinion regarding management and further investigation. Further inquiry into the minutiae of the presenting history revealed that the patient had previously removed a millipede from her shoe that day at school, having noticed some slightly painful irritation of the foot at the time. This irritation subsequently dissipated very quickly and the patient subsequently disregarded her potential millipede bite. However, © 2013 Royal Australasian College of Surgeons
Fig. 3. Resolution of trash foot appearance at 1 month follow-up.
while awaiting transfer to a ward bed, the patient herself searched for millipede bites on the internet. Her researches discovered that certain elements of millipede venom could cause a ‘burn’ with cutaneous appearances similar to the lesions she presented with. This new information was duly brought to the attention of her treating team, and the patient was accordingly managed conservatively by observation. At 1 month follow-up with the vascular surgery team, the discolouration of the initial lesions had largely disappeared (Fig. 3). There is a paucity of literature on ‘millipede burns’ in humans. In tropical countries such as Papua New Guinea, there have been reports of ‘burns’ caused by giant millipedes.1 Millipedes possess highly specialized exocrine glands that can secrete chemically irritant substances in response to perceived threats. Millipedes can also make use of cyanogenesis to produce hydrogen cyanide as a defence mechanism.2 It is postulated that the presence of quinone derivatives in millipede venom, such as toluquinone, p-benzoquinones and p-cresol cause the mahogany-black discolouration of the skin that so resembles necrosis.3 The mechanism of this mahogany discoloration is thought to involve an oxidation reaction as the quinone derivatives come into contact with skin lipids.4 Histological examination of a ‘millipede burn’ typically demonstrates only partial thickness epidermal necrosis with some adjacent inflammatory infiltrate.5 Although millipedes are common throughout many parts of the world, it appears that humans rarely come into close enough contact to encounter such a complication. Knowledge and recognition of the appearance of such ‘millipede burns’ will avoid misdiagnosis and unnecessary investigations.
References 1. Radford AJ. Giant millipede burns in Papua New Guinea. P.N.G. Med. J. 1976; 18: 138–41.
2. Eisner T, Alsop D, Hicks K, Meinwald J. Defensive secretions of millipedes. In: Bettin S (ed.). Arthropod Venoms. Berlin: Springer-Verlag, 1978; 41–72. 3. Shpall S, Frieden I. Mahogany discoloration of the skin due to the defensive secretion of a millipede. Pediatr. Dermatol. 1991; 8: 25–7. 4. Radford AJ. Millipede burns in man. Trop. Geogr. Med. 1975; 27: 279– 87. 5. Mason GH, Thomson HD, Fergin P, Anderson R. Mysterious lesions. Med. J. Aust. 1994; 160: 718–26.
Images for surgeons
Abhishek K. Verma,*† BSc (Med), MBBS Bernie Bourke,‡ MBBS, FRACS, DDU *School of Medicine and Public Health, University of Newcastle, †Department of Vascular Surgery, Gosford Hospital, and ‡Department of Vascular Surgery, Gosford Vascular Services Pty Ltd, Gosford, New South Wales, Australia doi: 10.1111/ans.12279
Giant neobladder stone Urolithiaisis is a recognized delayed complication of orthotopic neobladder construction. A stone in the neobladder may be asymptomatic and can be discovered as an incidental finding on a radiological investigation. However, when symptoms occur they may include severe lower abdominal pain, dysuria, haematuria or lower urinary tract symptoms. We describe a rare case of a giant neobladder stone which required open neocystolithotomy and fragmentation with hammer and chisel. A 60-year-old man presented with irritative lower urinary tract symptoms, lower abdominal pain, urinary incontinence and difficulty in self-catherization. Twenty years earlier, he underwent a radical cystoprostatectomy with orthotopic neobladder for urothelial carcinoma at another institution. He lost follow-up with his initial urologist as he has moved to another state. On physical examination, he was morbidly obese and abdominal examination was unremarkable apart from a lower midline abdominal scar. Laboratory investigations were positive for microhaematuria on urine analysis, but urine culture, urine cytology and renal functions were normal. A computed tomography of the abdomen and pelvis revealed a large round 12-cm calculus within the neobladder without evident of hydronephrosis (Fig. 1). He had an endoscopic evaluation for his lower urinary tract symptoms, which revealed a bulbar urethral stricture that was dilated. He proceeded to an open neocystolithotomy via an incision through the lower half of his previous midline scar. With the irrigation via the previously placed indwelling urinary catheter, the neobladder was distended and a vertical neocystolithotomy was performed carefully preserving the mesentery. A very hard 12-cm round stone was noted to be densely adherent to the mucosa of the neobladder and could not be removed intact despite enlarging the neocystotomy. Subsequently it was fragmented into smaller pieces with an orthopaedic chisel (Fig. 2). The neocystotomy was closed in two layers and a pelvic drain inserted. The pelvic drain was removed and patient was discharged with a 22-Fr indwelling catheter on day 2. The stone weighed 860 g (Fig. 3). Biochemical analysis of the stone showed it composed of magnesium ammonium phosphate (60%), calcium phosphate (32%) and calcium oxalate monohydrate (7%). After initially removing the urethral catheter at day 14, there was a continuous urine leak through the lower midline wound and the catheter was reinserted until the incision healed on day 28. Radical cystectomy with urinary diversion remains the standard of care for muscle invasive bladder cancer.1 Calculi are relatively uncommon following orthotopic urinary diversion. Its incidence has
Fig. 1. Coronal view of computed tomography abdomen and pelvis shows large stone in the neobladder.
been reported ranging between 0.5% and 7.0%.2–5 The aetiology of stone formation is multifactorial and includes the presence of infection, metabolic acidosis, stasis, mucus and foreign body. Most stones are composed primarily of struvite (magnesium ammonium phosphate) and are thought to be secondary to infection by urease producing organisms (Proteus, Klebsiella and Pseudomonas). The urease enzyme splits urea into ammonia and bicarbonate, which subsequently cause alkalinization of urine and promote the formation of struvite stone. Furthermore metabolic acidosis can lead to hypercalciuria, hypocitraturia, hyperoxaluria, hyperuricosuria and hyperphosphaturia, which may increase the stone risk. Similarly, urinary stasis, mucus and a foreign body have been implicated in the formation of stones.6–8 The presentation of a neobladder calculus may be asymptomatic. Without appropriate follow-up, these can grow to remarkable dimensions as illustrated in this case. Various surgical approaches have been described, including endoscopic neocystolitholapaxy, extracorporeal shock wave lithotripsy, percutaneous neocystolithotripsy and © 2013 Royal Australasian College of Surgeons