- Email: [email protected]
False positive diagnosis of malignant melanoma metastasis
218
Short reports and correspondence length needed for coverage of the periphery of the defect. Under these circumstances, there was always the risk of inadvertently dividing the flap too far distally, resulting in it being sutured under tension, and therefore making it more prone to wound dehiscence. In conclusion, we believe that the technique we have described here provides an easy and rapid method for identifying the exact site of division of the nasolabial flap at the time of the second stage of the procedure.
References
Figure 1 Large ulcerative squamous cell carcinoma of the floor-of-mouth and ventral tongue.
stitches, the stitches were removed, and the flaps were inset and sutured to the margin of the defect.
Discussion The exact site of division of a nasolabial flap is occasionally difficult to identify. This is due to several factors: firstly, the flap is still oedematous 2 to 3 weeks after the first stage, thus distorting anatomy; secondly, healing of the flap where it has been sutured to the defect makes the margins indistinct; and thirdly, it is difficult to determine the exact remaining margin of the defect because it is obstructed by the pedicle of the flap. Previously, we used to divide the flap at its exit from the buccal mucosa, and then trim it until we achieved the exact
1. Pers M. Cheek flaps in partial rhinoplasty. Scand J Plast Reconstr Surg 1967;1:37e42. 2. Maurer P, Eckert AW, Schubert J. Functional rehabilitation following resection of the floor of the mouth: the nasolabial flap revisited. J Craniomaxillofac Surg 2002;30:369e72. 3. Lazaridis N. Unilateral subcutaneous pedicled nasolabial island flap for anterior mouth floor reconstruction. J Oral Maxillofac Surg 2003;61:182e90. 4. Ioannides C, Fossion E. Nasolabial flap for the reconstruction of defects of the floor of the mouth. Int J Oral Maxillofac Surg 1991;20:40e3. 5. McGregor IA, McGregor FM. Cancer of the Face and Mouth. Edinburgh, Scotland: Churchill Livingstone; 1986. p. 423.
Mohamed A. Ellabban William J.C. Van Niekerk Taimur Shoaib Canniesburn Plastic Surgery Unit, Glasgow Royal Infirmary, 16 Alexandra Parade, Glasgow G31 2ER, UK E-mail address: [email protected] ª 2007 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2007.09.025
False positive diagnosis of malignant melanoma metastasis Malignant melanoma recurs in w33% of patients after treatment of the primary lesion and may metastasise to almost any organ or tissue with the risk of recurrence directly related to the stage at presentation.1 NICE guidelines2 recommend that patients should be managed as part of a specialist skin cancer multidisciplinary team but clinicians should still be aware of the possibility of false positive diagnoses. We present a series of four false positive diagnoses of metastatic malignant melanoma over a period of 15 years in the regional malignant melanoma centre at St. George’s Hospital.
Patient 1 (Clinical false positive)
Figure 2 Marking the exact site of division of the two-stage nasolabial flap by two nonabsorbable silk stitches at the exact site of division of each flap.
A 58-year-old gentleman presented in November 2005 with a malignant melanoma on his cheek and a soft tissue swelling in his neck. Our obvious concern was that the neck swelling could be a metastasis from the melanoma on
Short reports and correspondence
219
his right cheek. A fine needle aspiration (FNA) biopsy later confirmed this to be a Warthin’s tumour.
Patient 2 (False positive on CT scan) A 60-year-old lady had a wide local excision of a malignant melanoma (Breslow thickness 4 mm) from her left scapula and a sentinel node biopsy in her left axilla in April 2004. A follow-up computed tomography (CT) scan was performed in December 2004 to reassess a lesion in her liver but it also revealed a nodule in the lower lobe of her left lung which was diagnosed as a metastatic deposit. Based on this CT diagnosis, a wedge resection of the left lower lobe was performed. The histology confirmed a non-caseating granulomatous inflammation instead of a metastatic deposit.
Patient 3 (False positive on FNA) A 59-year-old gentleman presented in February 2004 with a malignant melanoma on his back (Breslow thickness 3.1 mm) and also left axillary and neck swellings. The patient underwent a wide local excision of the lesion and FNA of the left axilla which revealed metastatic melanoma. A staging CT scan showed left axillary lymphadenopathy and a bulky lower oesophagus of uncertain significance (Fig. 1). However, a left axillary dissection in March 2004 showed metastatic adenocarcinoma instead of melanoma. An oesophago-gastro-duodenoscopy biopsy subsequently diagnosed a poorly differentiated adenocarcinoma in the lower third of his oesophagus.
Patient 4 (False positive on CT and FNA) A 68-year-old gentleman initially presented in 1965 with a malignant melanoma on his left supraclavicular fossa. In September 2005, the patient developed a recurrence in his left neck and a modified left radical neck dissection was
Figure 2 High powered view of CT-guided FNA biopsy of pulmonary nodule from Patient 4 showing a dispersed population of atypical cells (binucleate and plasmacytoid cells) and also adjacent anthracotic pigment (a black pigment that mimics melanin). A left lower lobe lung resection was performed as this was consistent with metastatic malignant melanoma; however, histology from the resection established it to be a pulmonary hamartoma instead.
performed. A staging CT scan revealed a left lower lobe lung lesion and CT guided FNA confirmed metastatic malignant melanoma. However, a lung resection in November 2005 revealed the nodule to be a pulmonary hamartoma (Fig. 2).
Discussion FNA and CT are important investigations to confirm clinical suspicion when dealing with a chimeric entity such as metastatic malignant melanoma. FNA is a minimally invasive procedure that can diagnose metastatic malignant melanoma accurately and rapidly with a reported false positive rate of 1%.3 The role of CT in metastatic malignant melanoma has not been fully established but selective use in certain subgroups of patients with stage three disease may be useful.4 However, benign tumours, other synchronous malignancies or chronic granulomatous lesions (e.g. tuberculosis) should still be kept in mind as differential diagnoses to avoid the false positive diagnosis as shown by the four cases above. Misdiagnosis can lead to inappropriate treatment and considerable morbidity for the patient who has to undergo chemotherapy, radiotherapy or invasive surgery.
References
Figure 1 Staging CT scan showing a bulky lower oesophagus of uncertain significance from Patient 3. Other abnormalities were identified and further investigated but the significance of this abnormality only came to light after a cervical lymphadenectomy revealed that the lymph nodes contained metastatic adenocarcinoma rather than metastatic malignant melanoma.
1. Allen PJ, Coit DG. The surgical management of metastatic melanoma. Ann Surg Oncol 2002;9:762e70. 2. National Institute for Clinical Excellence. Improving outcomes for people with skin tumours including melanoma. Available from: http://www.nice.org.uk/page.aspx?o Z 265929; 2005 July [cited 1st May 2006]. 3. Rodrigues LK, Leong SP, Ljung BM, et al. Fine needle aspiration in the diagnosis of metastatic melanoma. J Am Acad Dermatol 2000;42:735e40.
220
Short reports and correspondence
4. Johnson TM, Fader DJ, Chang AE, et al. Computed tomography in staging of patients with melanoma metastatic to the regional nodes. Ann Surg Oncol 1997;4:396e402.
J. Lim Department of Cardiothoracic Surgery, John Radcliffe Hospital, Headley Way, Headington, Oxford OX3 9DU, UK E-mail address: [email protected] S. Vadodaria B.W.E.M. Powell Department of Plastic Surgery, St. George’s Healthcare NHS Trust, Blackshaw Road, Tooting, London SW17 0QT, UK ª 2007 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2007.09.028
Cleft palate repair with the use of osmotic expanders: a response We read with interest the recent preliminary report by Kobus whereby self-inflating tissue expanders were used in the primary surgical repair of 19 children with cleft palate.1 Although the raison d’e ˆtre behind using tissue expanders in the surgical management of the wide cleft palate is a compelling one, particularly with reference to limiting palatal scarring and the preservation of maxillary growth, this report appears to raise more questions than it answers. In particular, we have reservations as to the nature of the device used, the patient selection criteria adopted, and the surgical methodology employed. Austad first proposed an osmotically active self-inflating device based on a semipermeable silicone membrane containing a hyperosmolar solution of sodium chloride in 1982.2 Although he muted the potential for its application in cleft palate repair, the fundamental technical limitations proved insurmountable. Subsequently, Wiese developed an osmotically active hydrogel expander, whereby swelling was driven by an inert hygroscopic polymer.3 These devices have proved valuable in the surgical management of congenital anophthalmia, microphthalmia and cryptophthalmia.4e6 Experience with palatal tissue expansion is limited; Abramo et al. used acute intraoperative tissue expansion in the primary repair of a series of 12 large palatal clefts, incurring a single postoperative fistula.7 De Mey et al. reported the treatment of a large anterior palatal fistula by means of two custom-made silicone balloon implants with external filling ports.8 A further, albeit unsuccessful, case has been documented by Van Damme, who has extensively studied the effect of subperiosteal palatal expansion in cats using traditional balloon-type devices.9e11 With respect to tissue expansion in a confined anatomical location such as the palate, our elemental concern is one of
direction dependence. Standard balloon-type and, hitherto, osmotic expanders are isotropic, in that they expand equally in all directions. Clearly in the confines of a palatal cleft such a device is inherently at risk of extrusion e a potentially catastrophic complication. What is required is a device which allows directionally dependent swelling (i.e. is anisotropic) thereby facilitating obliteration of the cleft in a transverse direction but without the attendant risks of anteroposterior extrusion. Furthermore the ‘acute’ expansion technique used by Kobus is essentially a variant of rapid intraoperative expansion, as first described by Gibson in 1977 and popularised in the late 1980s by Sasaki.12,13 The technique remains controversial; whilst its proponents claim it to be highly effective clinically, its critics believe it to offer little benefit over undermining alone.14,15 However, evidence from porcine studies suggests that continuous skin expansion over a 3day period achieves significantly greater amounts of additional tissue than intraoperative expansion.16 We question whether such an accelerated expansion regime can be justified in children; this study required patients to be fed parenterally for the duration of the expansion period, and regular intraoral surveillance was necessary in order to detect possible tissue necrosis and thus pre-empt expander extrusion. Concerns over tissue viability necessitated early surgical intervention in an unspecified number of children. It is our opinion that the disadvantages of ‘super-quick’ expansion far outweigh any putative advantages. Over the past four years we have developed a unique hydrogel copolymer which exhibits controlled expansion both in terms of direction and rate.17 Whereas Kobus was constrained by a fixed acute expansion period whereby 98% swelling was achieved within 24 h, we have the capability of precisely tailoring the rate of expansion to the specific requirements of the clinical indication. The efficacy of our device has been verified in vivo by expanding porcine palatal tissue over a 6-week period. Unlike ‘acute’ tissue expansion, ‘chronic’ expansion induces profound biological effects in the expanded tissues; Johnson et al. introduced the term ‘biological creep’ to describe this generation of new tissue secondary to a chronic stress.18 Being at the nascency of developing a two-staged palatal repair by means of tissue expanders, we would favour restricting their clinical use to the widest palatal defects where the limitations of conventional repair are most evident in terms of fistulation, maxillary growth retardation and velopharyngeal incompetence. We have difficulty in condoning an experimental technique in a child with a narrow defect which could be adequately repaired by conventional methods. If the two-staged technique were to prove beneficial in wider defects, it might then be appropriate to consider, subject to ethical approval, a randomised controlled trial of the technique in children with narrower defects. Moreover, the mechanism of selecting patients for inclusion in this study was not made sufficiently clear; were they chosen sequentially, and if so, what type of cleft, if any, was excluded? Of note, the patient age range at surgery was beyond that at which we would aim to have achieved primary palatal cleft closure in the UK.19 Kobus conceded that this partly reflected the local patient referral pattern, although it may also have been influenced by other confounding factors including the
Short reports and correspondence length needed for coverage of the periphery of the defect. Under these circumstances, there was always the risk of inadvertently dividing the flap too far distally, resulting in it being sutured under tension, and therefore making it more prone to wound dehiscence. In conclusion, we believe that the technique we have described here provides an easy and rapid method for identifying the exact site of division of the nasolabial flap at the time of the second stage of the procedure.
References
Figure 1 Large ulcerative squamous cell carcinoma of the floor-of-mouth and ventral tongue.
stitches, the stitches were removed, and the flaps were inset and sutured to the margin of the defect.
Discussion The exact site of division of a nasolabial flap is occasionally difficult to identify. This is due to several factors: firstly, the flap is still oedematous 2 to 3 weeks after the first stage, thus distorting anatomy; secondly, healing of the flap where it has been sutured to the defect makes the margins indistinct; and thirdly, it is difficult to determine the exact remaining margin of the defect because it is obstructed by the pedicle of the flap. Previously, we used to divide the flap at its exit from the buccal mucosa, and then trim it until we achieved the exact
1. Pers M. Cheek flaps in partial rhinoplasty. Scand J Plast Reconstr Surg 1967;1:37e42. 2. Maurer P, Eckert AW, Schubert J. Functional rehabilitation following resection of the floor of the mouth: the nasolabial flap revisited. J Craniomaxillofac Surg 2002;30:369e72. 3. Lazaridis N. Unilateral subcutaneous pedicled nasolabial island flap for anterior mouth floor reconstruction. J Oral Maxillofac Surg 2003;61:182e90. 4. Ioannides C, Fossion E. Nasolabial flap for the reconstruction of defects of the floor of the mouth. Int J Oral Maxillofac Surg 1991;20:40e3. 5. McGregor IA, McGregor FM. Cancer of the Face and Mouth. Edinburgh, Scotland: Churchill Livingstone; 1986. p. 423.
Mohamed A. Ellabban William J.C. Van Niekerk Taimur Shoaib Canniesburn Plastic Surgery Unit, Glasgow Royal Infirmary, 16 Alexandra Parade, Glasgow G31 2ER, UK E-mail address: [email protected] ª 2007 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2007.09.025
False positive diagnosis of malignant melanoma metastasis Malignant melanoma recurs in w33% of patients after treatment of the primary lesion and may metastasise to almost any organ or tissue with the risk of recurrence directly related to the stage at presentation.1 NICE guidelines2 recommend that patients should be managed as part of a specialist skin cancer multidisciplinary team but clinicians should still be aware of the possibility of false positive diagnoses. We present a series of four false positive diagnoses of metastatic malignant melanoma over a period of 15 years in the regional malignant melanoma centre at St. George’s Hospital.
Patient 1 (Clinical false positive)
Figure 2 Marking the exact site of division of the two-stage nasolabial flap by two nonabsorbable silk stitches at the exact site of division of each flap.
A 58-year-old gentleman presented in November 2005 with a malignant melanoma on his cheek and a soft tissue swelling in his neck. Our obvious concern was that the neck swelling could be a metastasis from the melanoma on
Short reports and correspondence
219
his right cheek. A fine needle aspiration (FNA) biopsy later confirmed this to be a Warthin’s tumour.
Patient 2 (False positive on CT scan) A 60-year-old lady had a wide local excision of a malignant melanoma (Breslow thickness 4 mm) from her left scapula and a sentinel node biopsy in her left axilla in April 2004. A follow-up computed tomography (CT) scan was performed in December 2004 to reassess a lesion in her liver but it also revealed a nodule in the lower lobe of her left lung which was diagnosed as a metastatic deposit. Based on this CT diagnosis, a wedge resection of the left lower lobe was performed. The histology confirmed a non-caseating granulomatous inflammation instead of a metastatic deposit.
Patient 3 (False positive on FNA) A 59-year-old gentleman presented in February 2004 with a malignant melanoma on his back (Breslow thickness 3.1 mm) and also left axillary and neck swellings. The patient underwent a wide local excision of the lesion and FNA of the left axilla which revealed metastatic melanoma. A staging CT scan showed left axillary lymphadenopathy and a bulky lower oesophagus of uncertain significance (Fig. 1). However, a left axillary dissection in March 2004 showed metastatic adenocarcinoma instead of melanoma. An oesophago-gastro-duodenoscopy biopsy subsequently diagnosed a poorly differentiated adenocarcinoma in the lower third of his oesophagus.
Patient 4 (False positive on CT and FNA) A 68-year-old gentleman initially presented in 1965 with a malignant melanoma on his left supraclavicular fossa. In September 2005, the patient developed a recurrence in his left neck and a modified left radical neck dissection was
Figure 2 High powered view of CT-guided FNA biopsy of pulmonary nodule from Patient 4 showing a dispersed population of atypical cells (binucleate and plasmacytoid cells) and also adjacent anthracotic pigment (a black pigment that mimics melanin). A left lower lobe lung resection was performed as this was consistent with metastatic malignant melanoma; however, histology from the resection established it to be a pulmonary hamartoma instead.
performed. A staging CT scan revealed a left lower lobe lung lesion and CT guided FNA confirmed metastatic malignant melanoma. However, a lung resection in November 2005 revealed the nodule to be a pulmonary hamartoma (Fig. 2).
Discussion FNA and CT are important investigations to confirm clinical suspicion when dealing with a chimeric entity such as metastatic malignant melanoma. FNA is a minimally invasive procedure that can diagnose metastatic malignant melanoma accurately and rapidly with a reported false positive rate of 1%.3 The role of CT in metastatic malignant melanoma has not been fully established but selective use in certain subgroups of patients with stage three disease may be useful.4 However, benign tumours, other synchronous malignancies or chronic granulomatous lesions (e.g. tuberculosis) should still be kept in mind as differential diagnoses to avoid the false positive diagnosis as shown by the four cases above. Misdiagnosis can lead to inappropriate treatment and considerable morbidity for the patient who has to undergo chemotherapy, radiotherapy or invasive surgery.
References
Figure 1 Staging CT scan showing a bulky lower oesophagus of uncertain significance from Patient 3. Other abnormalities were identified and further investigated but the significance of this abnormality only came to light after a cervical lymphadenectomy revealed that the lymph nodes contained metastatic adenocarcinoma rather than metastatic malignant melanoma.
1. Allen PJ, Coit DG. The surgical management of metastatic melanoma. Ann Surg Oncol 2002;9:762e70. 2. National Institute for Clinical Excellence. Improving outcomes for people with skin tumours including melanoma. Available from: http://www.nice.org.uk/page.aspx?o Z 265929; 2005 July [cited 1st May 2006]. 3. Rodrigues LK, Leong SP, Ljung BM, et al. Fine needle aspiration in the diagnosis of metastatic melanoma. J Am Acad Dermatol 2000;42:735e40.
220
Short reports and correspondence
4. Johnson TM, Fader DJ, Chang AE, et al. Computed tomography in staging of patients with melanoma metastatic to the regional nodes. Ann Surg Oncol 1997;4:396e402.
J. Lim Department of Cardiothoracic Surgery, John Radcliffe Hospital, Headley Way, Headington, Oxford OX3 9DU, UK E-mail address: [email protected] S. Vadodaria B.W.E.M. Powell Department of Plastic Surgery, St. George’s Healthcare NHS Trust, Blackshaw Road, Tooting, London SW17 0QT, UK ª 2007 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2007.09.028
Cleft palate repair with the use of osmotic expanders: a response We read with interest the recent preliminary report by Kobus whereby self-inflating tissue expanders were used in the primary surgical repair of 19 children with cleft palate.1 Although the raison d’e ˆtre behind using tissue expanders in the surgical management of the wide cleft palate is a compelling one, particularly with reference to limiting palatal scarring and the preservation of maxillary growth, this report appears to raise more questions than it answers. In particular, we have reservations as to the nature of the device used, the patient selection criteria adopted, and the surgical methodology employed. Austad first proposed an osmotically active self-inflating device based on a semipermeable silicone membrane containing a hyperosmolar solution of sodium chloride in 1982.2 Although he muted the potential for its application in cleft palate repair, the fundamental technical limitations proved insurmountable. Subsequently, Wiese developed an osmotically active hydrogel expander, whereby swelling was driven by an inert hygroscopic polymer.3 These devices have proved valuable in the surgical management of congenital anophthalmia, microphthalmia and cryptophthalmia.4e6 Experience with palatal tissue expansion is limited; Abramo et al. used acute intraoperative tissue expansion in the primary repair of a series of 12 large palatal clefts, incurring a single postoperative fistula.7 De Mey et al. reported the treatment of a large anterior palatal fistula by means of two custom-made silicone balloon implants with external filling ports.8 A further, albeit unsuccessful, case has been documented by Van Damme, who has extensively studied the effect of subperiosteal palatal expansion in cats using traditional balloon-type devices.9e11 With respect to tissue expansion in a confined anatomical location such as the palate, our elemental concern is one of
direction dependence. Standard balloon-type and, hitherto, osmotic expanders are isotropic, in that they expand equally in all directions. Clearly in the confines of a palatal cleft such a device is inherently at risk of extrusion e a potentially catastrophic complication. What is required is a device which allows directionally dependent swelling (i.e. is anisotropic) thereby facilitating obliteration of the cleft in a transverse direction but without the attendant risks of anteroposterior extrusion. Furthermore the ‘acute’ expansion technique used by Kobus is essentially a variant of rapid intraoperative expansion, as first described by Gibson in 1977 and popularised in the late 1980s by Sasaki.12,13 The technique remains controversial; whilst its proponents claim it to be highly effective clinically, its critics believe it to offer little benefit over undermining alone.14,15 However, evidence from porcine studies suggests that continuous skin expansion over a 3day period achieves significantly greater amounts of additional tissue than intraoperative expansion.16 We question whether such an accelerated expansion regime can be justified in children; this study required patients to be fed parenterally for the duration of the expansion period, and regular intraoral surveillance was necessary in order to detect possible tissue necrosis and thus pre-empt expander extrusion. Concerns over tissue viability necessitated early surgical intervention in an unspecified number of children. It is our opinion that the disadvantages of ‘super-quick’ expansion far outweigh any putative advantages. Over the past four years we have developed a unique hydrogel copolymer which exhibits controlled expansion both in terms of direction and rate.17 Whereas Kobus was constrained by a fixed acute expansion period whereby 98% swelling was achieved within 24 h, we have the capability of precisely tailoring the rate of expansion to the specific requirements of the clinical indication. The efficacy of our device has been verified in vivo by expanding porcine palatal tissue over a 6-week period. Unlike ‘acute’ tissue expansion, ‘chronic’ expansion induces profound biological effects in the expanded tissues; Johnson et al. introduced the term ‘biological creep’ to describe this generation of new tissue secondary to a chronic stress.18 Being at the nascency of developing a two-staged palatal repair by means of tissue expanders, we would favour restricting their clinical use to the widest palatal defects where the limitations of conventional repair are most evident in terms of fistulation, maxillary growth retardation and velopharyngeal incompetence. We have difficulty in condoning an experimental technique in a child with a narrow defect which could be adequately repaired by conventional methods. If the two-staged technique were to prove beneficial in wider defects, it might then be appropriate to consider, subject to ethical approval, a randomised controlled trial of the technique in children with narrower defects. Moreover, the mechanism of selecting patients for inclusion in this study was not made sufficiently clear; were they chosen sequentially, and if so, what type of cleft, if any, was excluded? Of note, the patient age range at surgery was beyond that at which we would aim to have achieved primary palatal cleft closure in the UK.19 Kobus conceded that this partly reflected the local patient referral pattern, although it may also have been influenced by other confounding factors including the