- Email: [email protected]
Why do cystic duct clips migrate into the common bile duct?
dorsum of the hands in transplant patients), these significantly reduce the morbidity from skin cancer in this high-risk population and save lives.
face
or
measures could
*Jane M McGregor, Charlotte M Proby *Department of Photobiology, St John’s Institute of Dermatology, St Thomas’ Hospital, London SE1 7EH, UK; and ICRF Skin Tumour Laboratory, Royal London Hospital, London 1 Birkeland
SA, Storm HH, Lamm LU,
al. Cancer risk after 1964-1986. Int J Cancer 1995;
SCC.‘-3 Regular surveillance of patients with skin problems and easy access of all patients to a dermatologist is advised, as well as early biopsy of suspicious lesions.’3 Resurfacing the back of the hand can be a successful treatment for carefully selected patients with multiple SCC on the back of the hand, and acitretin, an oral retinoid, seems to be effective in the prevention of cutaneous SCC in recipients with severe lesions.’
et
transplantation in the Nordic countries
60: 183-90. 2 Glover MT, Niranjan N, Kwan JT, et al. Non-melanoma skin cancer in renal transplant recipients: the extent of the problem and a strategy for management. Br J Plast Surg 1994; 47: 86-89. 3 Hartvelt MM, Bouwes Bavincke JN, Koote AMM, et al. Incidence of skin cancer after renal transplantation in the Netherlands. Transplantation 1990; 49: 506-09. 4 McGregor JM, Morris RH, Smith CH, MacDonald DM. Skin cancer morbidity amongst renal allograft recipients—a 25 year retrospective follow-up study. Br J Dermatol 1995; 133: 40 (abstr). 5 UK Skin Cancer Prevention Working Parry. Sunshine and skin cancer: consensus statement. BMA News Review 1994; 20: 12.
*J N Bouwes Netherlands
1
2
3
4
SIR-London and colleagues nicely confirm the cumulative risk of cutaneous SCC in allograft recipients after in a typical transplant population from a temperate area of northern Europe. In Leeds, UK, the risk of cutaneous SCC increased steadily from about 3 years post-transplant to over 6% by 10 years and 30% by 20 years. In Leiden, Netherlands, in a group of 764 patients who received a renal allograft between 1966 and 1988, these percentages were 7% by 10 years and 35% by 20 years,
transplantation
1
respectively.’
London and colleagues give a descriptive analysis of the percentages of different tumours developing in allograft recipients: 53% were cutaneous. They also assessed potential risk factors for developing neoplastic disease, but they analysed all tumours together. In their calculations only age at transplantation and length of pretransplant dialysis seemed to be important. They conclude that immunological differences between donor and recipient do not seem important in terms of neoplasia, despite their clinical significance in rejection. An important drawback of their study is that the aetiology of the various tumours is not identical. For the analysis of risk factors we believe that particular tumour types should be the focus, rather than to try to cover the overall picture. We studied risk factors for cutaneous tumours and analysed the risk factors for SCC and basal cell carcinomas (BCC) separately. Mismatching between the donor and recipient for HLA-B antigens was associated with an increased risk of cutaneous SCC.= Additional risk factors that were identified for cutaneous SCC in allograft recipients were the age of the patient,3 duration of immunosuppressive therapy, 1,3 exposure to sunlight/,3 infection with human papillomaviruses/,3 immune response against human papillomaviruses,’ HLA-phenotype of the recipient,2 and HLA-DR homozygosity.2 Risk factors for BCC were basically the same, although some differences were noted, mainly in the magnitude of the effect.1-4 In the transplant population compared with the healthy population the risk of BCC is less increased than the risk of SCC, resulting in a reverse of the SCC to BCC ratio,’ and the localisation of both tumours is slightly different.’1 We agree with London and colleagues that cutaneous SCC is a major cause of post-transplant morbidity, but we do not agree that little progress has been made towards understanding or reducing this risk. Exposure to sunlight and infection with human papillomaviruses are the major environmental risk factors for cutaneous SCC.’-’ Sunprotective measures are important to reduce the risk of
Bavinck, B J Vermeer
Department of Dermatology, University Hospital Leiden, 2333 AA Leiden,
5
Hartevelt MM, Bouwes Bavinck JN, Kootte AMM, Vermeer BJ, Vandenbroucke JP. Incidence of skin cancer after renal transplantation in the Netherlands. Transplantation 1990; 49: 506-09. Bouwes Bavinck JN, Vermeer BJ, van der Woude FJ, et al. Relation between skin cancer and HLA antigens in renal-transplant recipients. N Engl J Med 1991; 325: 843-48. Bouwes Bavinck JN, Vermeer BJ, Claas FHJ, ter Schegget J, van der Woude FJ. Skin cancer and renal transplantation. J Nephrology 1994; 7: 261-67. Bouwes Bavinck JN, Gissmann L, Claas FHJ, et al. Relation between skin cancer, humoral responses to human papillomaviruses, and HLA class II molecules in renal transplant recipients. J Immunol 1993; 151: 1579-86. Bouwes Bavinck JN, Tieben LM, van der Woude FJ, et al. Prevention of skin cancer and reduction of keratotic skin lesions during acitretin therapy in renal-transplant recipients: a double blind, placebocontrolled study. J Clin Oncol 1995; 13: 1933-38.
Why do cystic duct clips migrate into the common
bile duct?
SiR-Laparoscopic cholecystectomy has been associated a variety of unexpected complications,’ including migration of metal clips into the common bile duct after operation. One suggested cause of clip migration is improper application of the clips, which does not completely close the cystic duct and allows the development of a biloma. This does not explain the observation of clip migration without biloma. An alternative is that the clip may erode slowly through the duct, eventually coming to lie within the lumen of the biliary tract. This hypothesis cannot, however, explain the migration of two clips (which are usually applied) through the cystic duct and into the biliary lumen, which has been reported in several cases. We propose that clip migration happens in four stages: the clipped cystic duct is pressed by surrounding tissue, such as the liver (figure a); the cystic duct with attached clips is then inverted into the lumen of the common bile duct (figure b); inversion of the cystic duct results in necrosis in the common bile duct; and finally, the necrosed stump of the cystic duct becomes covered by surrounding tissues
with
Figure: Proposed
sequence of
clip migration 965
(figure c). In the absence of the fourth stage, a biliary fistula leading to a biloma will be found. Our hypothesis also explains one cause of stone formation in the common bile duct following cholecystectomy. Suture material is known to be a nidus for stone formation after traditional cholecystectomy for cholelithiasis. There have been numerous reports of silk sutures within common bile duct stones,4,5 but why silk sutures migrate into the common bile duct is uncertain. Even in cholecystectomy under open laparotomy, suture materials could migrate into the common bile duct if the events described above were to occur. This migration would allow bile crystals to adhere to the ligatures with subsequent stone formation. To avoid migration of suture material and clips, and subsequent stone formation, absorbable suture material should be used for ligating the cystic duct. If this is not an option, the cystic duct should be sutured as far from the common bile duct as possible.
Fetal movements, other than breathing have also been reported to be reduced. The striking "promotion" is fat deposition, which explains the increase in birth weight in these babies. Garner’s discussion of diabetic retinopathy lacks clarity. Women with pregestational stable glycaemic control with acceptable HbA, measurements who have undergone treatment for retinopathy run little risk of activatihg their retinopathy. In our own series, seven women with photocoagulated proliferative retinopathy have maintained stable vision of 6/9 or better for 2 years or more after the pregnancy. This finding contrasts with the combination of poor pregestational glycaemic control in the presence of background retinopathy, where three of 49 with diabetic
women.
movement
background retinopathy developed proliferative retinopathy requiring laser treatment. It is in the latter group that retinopathy can progress to proliferative retinopathy and visual impairment.
*Kazuya Kitamura, Toshiharu Yamaguchi, Hirohisa Nakatani, Daisuke Ichikawa, Masataka Shimotsuma, Tetsuro Yamane, Toshio Takahashi
Clara
Lowy
Unit of
Endocrinology
First Department of
1
Surgery, Kyoto
Prefectural
University of Medicine, Kamigyo-ku,
Kyoto 602, Japan 2 1
2 3
4
5
Wilson P, Leese T, Morgan WP, Kelly JF, Brigg JK. Elective laparoscopic cholcystectomy for "all-comers". Lancet 1991; 338: 795-97. Onghena T, Vereecken L, Dwey K, Loon C. Common bile duct foreign body: an unusual case. Surg Laparosc Endosc 1992; 2: 8-10. Matsuura T, Kanisawa Y, Sato T, Saito T, Hirata K. Migration of "endo-clips" into common bile duct after laparoscopic cholecystectomy. Lancet 1992; 340: 306. Homans J. Silk suture within gallbladder stones. Ann Surg 1897; 26: 114. Rees BI, Jacob G. Silk sutures in the common bile duct. BMJ 1977; 4: 1265.
Type I diabetes SiR-Some p
157)
are
and pregnancy
points made by Garner in misleading and/or incorrect.
his review
(July 15,
He states that the stillbirth incidence is greatest after 36 weeks. A UK study of 773 diabetic pregnancies, collated 1979-80, reported 22 stillbirths.’ All were 36 weeks or less in gestation, except for two whose gestation was not known but who weighed 3-4 kg or more. At the British Congress of Obstetrics and Gynaecology (Dublin, June 1995), McAuliffe et al presented data from the National Maternity Hospital, Dublin. 148 of 373 women had spontaneous onset of labour after 38 weeks; 84% of these full-termers had a normal vaginal delivery, with a perinatal mortality of 13-5/1000. Two still-births occurred (at 40 and 41 weeks). The Dublin experience is probably unique since the unit has adopted a strict policy of term spontaneous onset vaginal delivery. Allowing pregnancies to continue to term has to be set against the risk of an induced preterm delivery. In most series, approximately half of the women have either an elected or intrapartum caesarean section after a failed induction. Preterm delivery exposes a neonate to the complications of prematurity. The Swedish survey of insulin-dependent women2 found complications of prematurity and maternal glycaemic control to be independent risk factors for neonatal morbidity, and perinatal mortality, but no mention was made of excess stillbirths after 36 weeks. The concept that the foetus is growth-promoted is misleading, since it suggests that fetal development is advanced. Crown-rump length and lung maturation may be retarded and the incidence of respiratory distress syndrome at a given gestational age is increased in infants born to 966
and Diabetes, St Thomas’ Hospital, London SE1 7EH, UK
Beard RW, Goldschmidt J. Congenital malformations in babies of diabetic mothers. Diabet Med 1986; 3: 458-62. Hanson U, Persson B. Outcome of pregnancies complicated by type I insulin dependent diabetes in Sweden: acute pregnancy complications, neonatal mortality and morbidity. Am J Perinatology 1993; 10: 330-33.
Lowy C,
Author’s
reply
SiR-Two objectives of my review on type I diabetes mellitus in pregnancy were to present a global perspective, and to cover controversial areas, so I am pleased that Lowy has taken me to task on three important issues. The first issue is: when is a stillbirth most likely to occur during a pregnancy? The UK survey (1979-80) suggested that the majority of stillbirths occurred before 36 weeks.’ The data from this survey, which was conducted by mail, can be criticised in that, of 1403 pregnant diabetic women identified on first mailing, data was available only on 888 at foiled up, of whom 664 were "established" diabetics (? type I and type II diabetics). Thus, unfortunately, data were missing on more than a third of the pregnant diabetics initially identified. In addition the survey was conducted over 15 years ago, at a time when maternal/foetal surveillance was different. More recent large cohort series of purely type I diabetics still suggest that more stillbirths occur after 36 weeks than before. Lagrew et al documented three stillbirths in 614 type I diabetic pregnancies (37, 37, and 33 weeks);’ Landon et al reported one stillbirth among 114 pregnancies (37 weeks);3 and our own experience (1979-1994) has been five stillbirths in 372 pregnancies (39, 38, 38, 25, and 27 weeks). Of note in our series is that the late stillbirths occurred in non-compliant diabetic women, with poor glycaemic control and non-attendance for foetal monitoring, whereas the early stillbirths occurred in white class F diabetics with prepregnancy hypertension and early onset pre-eclampsia.’’ Whether the difference in the postal survey compared with the cohort series reflects regional variations or changes in foetal surveillance is difficult to judge. However, I fully agree with Lowy that the take-home message is the same: well-controlled type I diabetics with good maternal/foetal monitoring should be taken to term and delivered at a time when vaginal delivery is optimised, thus avoiding failed induction and the neonatal morbidity associated with prematurity. Lowy believes that the concept that the foetus is growth promoted is misleading, as it implies that foetal development is advanced. In my review I did not imply this association. My own departments of obstetrics/
face
or
measures could
*Jane M McGregor, Charlotte M Proby *Department of Photobiology, St John’s Institute of Dermatology, St Thomas’ Hospital, London SE1 7EH, UK; and ICRF Skin Tumour Laboratory, Royal London Hospital, London 1 Birkeland
SA, Storm HH, Lamm LU,
al. Cancer risk after 1964-1986. Int J Cancer 1995;
SCC.‘-3 Regular surveillance of patients with skin problems and easy access of all patients to a dermatologist is advised, as well as early biopsy of suspicious lesions.’3 Resurfacing the back of the hand can be a successful treatment for carefully selected patients with multiple SCC on the back of the hand, and acitretin, an oral retinoid, seems to be effective in the prevention of cutaneous SCC in recipients with severe lesions.’
et
transplantation in the Nordic countries
60: 183-90. 2 Glover MT, Niranjan N, Kwan JT, et al. Non-melanoma skin cancer in renal transplant recipients: the extent of the problem and a strategy for management. Br J Plast Surg 1994; 47: 86-89. 3 Hartvelt MM, Bouwes Bavincke JN, Koote AMM, et al. Incidence of skin cancer after renal transplantation in the Netherlands. Transplantation 1990; 49: 506-09. 4 McGregor JM, Morris RH, Smith CH, MacDonald DM. Skin cancer morbidity amongst renal allograft recipients—a 25 year retrospective follow-up study. Br J Dermatol 1995; 133: 40 (abstr). 5 UK Skin Cancer Prevention Working Parry. Sunshine and skin cancer: consensus statement. BMA News Review 1994; 20: 12.
*J N Bouwes Netherlands
1
2
3
4
SIR-London and colleagues nicely confirm the cumulative risk of cutaneous SCC in allograft recipients after in a typical transplant population from a temperate area of northern Europe. In Leeds, UK, the risk of cutaneous SCC increased steadily from about 3 years post-transplant to over 6% by 10 years and 30% by 20 years. In Leiden, Netherlands, in a group of 764 patients who received a renal allograft between 1966 and 1988, these percentages were 7% by 10 years and 35% by 20 years,
transplantation
1
respectively.’
London and colleagues give a descriptive analysis of the percentages of different tumours developing in allograft recipients: 53% were cutaneous. They also assessed potential risk factors for developing neoplastic disease, but they analysed all tumours together. In their calculations only age at transplantation and length of pretransplant dialysis seemed to be important. They conclude that immunological differences between donor and recipient do not seem important in terms of neoplasia, despite their clinical significance in rejection. An important drawback of their study is that the aetiology of the various tumours is not identical. For the analysis of risk factors we believe that particular tumour types should be the focus, rather than to try to cover the overall picture. We studied risk factors for cutaneous tumours and analysed the risk factors for SCC and basal cell carcinomas (BCC) separately. Mismatching between the donor and recipient for HLA-B antigens was associated with an increased risk of cutaneous SCC.= Additional risk factors that were identified for cutaneous SCC in allograft recipients were the age of the patient,3 duration of immunosuppressive therapy, 1,3 exposure to sunlight/,3 infection with human papillomaviruses/,3 immune response against human papillomaviruses,’ HLA-phenotype of the recipient,2 and HLA-DR homozygosity.2 Risk factors for BCC were basically the same, although some differences were noted, mainly in the magnitude of the effect.1-4 In the transplant population compared with the healthy population the risk of BCC is less increased than the risk of SCC, resulting in a reverse of the SCC to BCC ratio,’ and the localisation of both tumours is slightly different.’1 We agree with London and colleagues that cutaneous SCC is a major cause of post-transplant morbidity, but we do not agree that little progress has been made towards understanding or reducing this risk. Exposure to sunlight and infection with human papillomaviruses are the major environmental risk factors for cutaneous SCC.’-’ Sunprotective measures are important to reduce the risk of
Bavinck, B J Vermeer
Department of Dermatology, University Hospital Leiden, 2333 AA Leiden,
5
Hartevelt MM, Bouwes Bavinck JN, Kootte AMM, Vermeer BJ, Vandenbroucke JP. Incidence of skin cancer after renal transplantation in the Netherlands. Transplantation 1990; 49: 506-09. Bouwes Bavinck JN, Vermeer BJ, van der Woude FJ, et al. Relation between skin cancer and HLA antigens in renal-transplant recipients. N Engl J Med 1991; 325: 843-48. Bouwes Bavinck JN, Vermeer BJ, Claas FHJ, ter Schegget J, van der Woude FJ. Skin cancer and renal transplantation. J Nephrology 1994; 7: 261-67. Bouwes Bavinck JN, Gissmann L, Claas FHJ, et al. Relation between skin cancer, humoral responses to human papillomaviruses, and HLA class II molecules in renal transplant recipients. J Immunol 1993; 151: 1579-86. Bouwes Bavinck JN, Tieben LM, van der Woude FJ, et al. Prevention of skin cancer and reduction of keratotic skin lesions during acitretin therapy in renal-transplant recipients: a double blind, placebocontrolled study. J Clin Oncol 1995; 13: 1933-38.
Why do cystic duct clips migrate into the common
bile duct?
SiR-Laparoscopic cholecystectomy has been associated a variety of unexpected complications,’ including migration of metal clips into the common bile duct after operation. One suggested cause of clip migration is improper application of the clips, which does not completely close the cystic duct and allows the development of a biloma. This does not explain the observation of clip migration without biloma. An alternative is that the clip may erode slowly through the duct, eventually coming to lie within the lumen of the biliary tract. This hypothesis cannot, however, explain the migration of two clips (which are usually applied) through the cystic duct and into the biliary lumen, which has been reported in several cases. We propose that clip migration happens in four stages: the clipped cystic duct is pressed by surrounding tissue, such as the liver (figure a); the cystic duct with attached clips is then inverted into the lumen of the common bile duct (figure b); inversion of the cystic duct results in necrosis in the common bile duct; and finally, the necrosed stump of the cystic duct becomes covered by surrounding tissues
with
Figure: Proposed
sequence of
clip migration 965
(figure c). In the absence of the fourth stage, a biliary fistula leading to a biloma will be found. Our hypothesis also explains one cause of stone formation in the common bile duct following cholecystectomy. Suture material is known to be a nidus for stone formation after traditional cholecystectomy for cholelithiasis. There have been numerous reports of silk sutures within common bile duct stones,4,5 but why silk sutures migrate into the common bile duct is uncertain. Even in cholecystectomy under open laparotomy, suture materials could migrate into the common bile duct if the events described above were to occur. This migration would allow bile crystals to adhere to the ligatures with subsequent stone formation. To avoid migration of suture material and clips, and subsequent stone formation, absorbable suture material should be used for ligating the cystic duct. If this is not an option, the cystic duct should be sutured as far from the common bile duct as possible.
Fetal movements, other than breathing have also been reported to be reduced. The striking "promotion" is fat deposition, which explains the increase in birth weight in these babies. Garner’s discussion of diabetic retinopathy lacks clarity. Women with pregestational stable glycaemic control with acceptable HbA, measurements who have undergone treatment for retinopathy run little risk of activatihg their retinopathy. In our own series, seven women with photocoagulated proliferative retinopathy have maintained stable vision of 6/9 or better for 2 years or more after the pregnancy. This finding contrasts with the combination of poor pregestational glycaemic control in the presence of background retinopathy, where three of 49 with diabetic
women.
movement
background retinopathy developed proliferative retinopathy requiring laser treatment. It is in the latter group that retinopathy can progress to proliferative retinopathy and visual impairment.
*Kazuya Kitamura, Toshiharu Yamaguchi, Hirohisa Nakatani, Daisuke Ichikawa, Masataka Shimotsuma, Tetsuro Yamane, Toshio Takahashi
Clara
Lowy
Unit of
Endocrinology
First Department of
1
Surgery, Kyoto
Prefectural
University of Medicine, Kamigyo-ku,
Kyoto 602, Japan 2 1
2 3
4
5
Wilson P, Leese T, Morgan WP, Kelly JF, Brigg JK. Elective laparoscopic cholcystectomy for "all-comers". Lancet 1991; 338: 795-97. Onghena T, Vereecken L, Dwey K, Loon C. Common bile duct foreign body: an unusual case. Surg Laparosc Endosc 1992; 2: 8-10. Matsuura T, Kanisawa Y, Sato T, Saito T, Hirata K. Migration of "endo-clips" into common bile duct after laparoscopic cholecystectomy. Lancet 1992; 340: 306. Homans J. Silk suture within gallbladder stones. Ann Surg 1897; 26: 114. Rees BI, Jacob G. Silk sutures in the common bile duct. BMJ 1977; 4: 1265.
Type I diabetes SiR-Some p
157)
are
and pregnancy
points made by Garner in misleading and/or incorrect.
his review
(July 15,
He states that the stillbirth incidence is greatest after 36 weeks. A UK study of 773 diabetic pregnancies, collated 1979-80, reported 22 stillbirths.’ All were 36 weeks or less in gestation, except for two whose gestation was not known but who weighed 3-4 kg or more. At the British Congress of Obstetrics and Gynaecology (Dublin, June 1995), McAuliffe et al presented data from the National Maternity Hospital, Dublin. 148 of 373 women had spontaneous onset of labour after 38 weeks; 84% of these full-termers had a normal vaginal delivery, with a perinatal mortality of 13-5/1000. Two still-births occurred (at 40 and 41 weeks). The Dublin experience is probably unique since the unit has adopted a strict policy of term spontaneous onset vaginal delivery. Allowing pregnancies to continue to term has to be set against the risk of an induced preterm delivery. In most series, approximately half of the women have either an elected or intrapartum caesarean section after a failed induction. Preterm delivery exposes a neonate to the complications of prematurity. The Swedish survey of insulin-dependent women2 found complications of prematurity and maternal glycaemic control to be independent risk factors for neonatal morbidity, and perinatal mortality, but no mention was made of excess stillbirths after 36 weeks. The concept that the foetus is growth-promoted is misleading, since it suggests that fetal development is advanced. Crown-rump length and lung maturation may be retarded and the incidence of respiratory distress syndrome at a given gestational age is increased in infants born to 966
and Diabetes, St Thomas’ Hospital, London SE1 7EH, UK
Beard RW, Goldschmidt J. Congenital malformations in babies of diabetic mothers. Diabet Med 1986; 3: 458-62. Hanson U, Persson B. Outcome of pregnancies complicated by type I insulin dependent diabetes in Sweden: acute pregnancy complications, neonatal mortality and morbidity. Am J Perinatology 1993; 10: 330-33.
Lowy C,
Author’s
reply
SiR-Two objectives of my review on type I diabetes mellitus in pregnancy were to present a global perspective, and to cover controversial areas, so I am pleased that Lowy has taken me to task on three important issues. The first issue is: when is a stillbirth most likely to occur during a pregnancy? The UK survey (1979-80) suggested that the majority of stillbirths occurred before 36 weeks.’ The data from this survey, which was conducted by mail, can be criticised in that, of 1403 pregnant diabetic women identified on first mailing, data was available only on 888 at foiled up, of whom 664 were "established" diabetics (? type I and type II diabetics). Thus, unfortunately, data were missing on more than a third of the pregnant diabetics initially identified. In addition the survey was conducted over 15 years ago, at a time when maternal/foetal surveillance was different. More recent large cohort series of purely type I diabetics still suggest that more stillbirths occur after 36 weeks than before. Lagrew et al documented three stillbirths in 614 type I diabetic pregnancies (37, 37, and 33 weeks);’ Landon et al reported one stillbirth among 114 pregnancies (37 weeks);3 and our own experience (1979-1994) has been five stillbirths in 372 pregnancies (39, 38, 38, 25, and 27 weeks). Of note in our series is that the late stillbirths occurred in non-compliant diabetic women, with poor glycaemic control and non-attendance for foetal monitoring, whereas the early stillbirths occurred in white class F diabetics with prepregnancy hypertension and early onset pre-eclampsia.’’ Whether the difference in the postal survey compared with the cohort series reflects regional variations or changes in foetal surveillance is difficult to judge. However, I fully agree with Lowy that the take-home message is the same: well-controlled type I diabetics with good maternal/foetal monitoring should be taken to term and delivered at a time when vaginal delivery is optimised, thus avoiding failed induction and the neonatal morbidity associated with prematurity. Lowy believes that the concept that the foetus is growth promoted is misleading, as it implies that foetal development is advanced. In my review I did not imply this association. My own departments of obstetrics/