The aim of this study was to determine whether rapidly acquired MRI sequences, taking less than 5 min imaging time, can accurately characterise renal masses. All patients found to have a renal space-occupying lesion on CT or ultrasound were asked to participate in a prospective study using rapidly acquired MRI. The MRI technique was performed on a GE Signa (General Electric, Milwaukee, Wis.) 1.5 T magnet using breath-hold coronal and axial T1 GRASS (fast spoiled gradient-recalled acquisition into steady state, FSPGR/30/90) and axial T2 fast spin-echo sequences. The results were analysed by two radiologists unaware of the CT or ultrasound findings. The CT/US was independently viewed by a third radiologist. Lesions were characterised as simple cysts, indeterminate or solid. The MR and CT/US results were correlated and the sensitivity and specificity of MR for the characterisation of simple cysts and solid renal masses calculated. A total of 144 lesions (68 patients; 29 women 39 men, age range 32–78 years, average age 60 years) were studied: 111 simple cysts; 3 hyperdense cysts; 26 renal cell carcinomas; and 4 indeterminate lesions on CT/US. There was agreement between the CT/US and MRI in 82 % of cases. All renal cell carcinomas were correctly characterised on MRI. Of simple cysts, 79 % were correctly identified using this technique. Breath-hold MRI performed in less than 5 min can accurately characterise the majority of renal masses. It is 100 % sensitive in the characterisation of renal carcinoma, and it correctly identified approximately 80 % of simple cysts. If used at the time a renal mass is detected on MRI, it would reduce the need for further investigation of the majority of incidentally detected lesions which are simple cysts.

In acromegaly, symptomatic carpal tunnel syndrome has been reported to occur in up to 64% of patients at presentation (1), but more than 80% of patients have subclinical abnormalities on nerve conduction studies (2). Most of these patients show significant improvement after circulating growth hormone levels are decreased (1, 3-6); however, the underlying pathogenic mechanisms are unknown (7, 8). In patients without acromegaly, advances in magnetic resonance imaging (MRI) techniques have made imaging of the wrist joint and carpal tunnel feasible, allowing assessment of pathologic processes involving the nerve itself and the carpal tunnel contents (9-11). On axial MR images, the median nerve is easily seen as a round or flattened structure of intermediate signal intensity (Figure 1); its diameter is normally relatively constant at the level of the distal radius, the proximal carpal tunnel (at the level of the pisiform bone), and the distal carpal tunnel (at the hook of the hamate bone). Reported MRI findings associated with carpal tunnel syndrome in patients without acromegaly include swelling and flattening of the median nerve within the carpal tunnel, increased signal intensity on T2-weighted images due to increased edema, and palmar bowing of the flexor retinaculum (12, 13). It is unknown whether these changes also occur in acromegalic patients with the carpal tunnel syndrome. Figure 1. Cross-sectional diagram ( top ) and T2-weighted axial magnetic resonance imaging scan ( bottom ) of the wrist and carpal tunnel at the level of the hamate bone. We sought to elucidate the pathology of median neuropathy in acromegaly by using MRI and to assess morphologic responses after decreasing levels of circulating growth hormone and insulin-like growth factor I (IGF-I). Methods Nine consecutive patients with acromegaly were studied at presentation and 6 months after treatment with transsphenoidal surgery, pituitary irradiation, or somatostatin analogues, alone or in combination. Acromegaly was diagnosed according to established criteria (14). Serum growth hormone was measured at the North East Thames Regional Immunoassay Laboratory by using an immunoradiometric assay (interassay and intra-assay coefficient of variation<8%), and serum IGF-I was measured by using an in-house radioimmunoassay (interassay and intra-assay coefficient of variation<10%). All patients were euthyroid or were taking adequate thyroxine replacement. Four patients had clinical symptoms suggestive of median neuropathy, and five were asymptomatic. The study was approved by the local Ethical Research Committee, and all patients gave written informed consent. Because sequential study enabled each patient to act as his or her own control, a control group of patients with idiopathic carpal tunnel syndrome was not studied. Magnetic resonance imaging was performed by using a GE Signa Horizon 1.5T MRI unit (GE Medical Systems, Milwaukee, Wisconsin). The patients were examined while prone with the arm above the head. Images were obtained by using a small surface coil with the wrist joint positioned in the middle of the coil. The wrist was secured with restraining bands to prevent movement, and the fingers were kept extended to prevent the lumbrical muscles from slipping into the carpal tunnel with finger flexion. The more symptomatic wrist was studied in the four symptomatic patients; in the five asymptomatic patients, the dominant hand was studied. As was done in studies of idiopathic carpal tunnel syndrome (12), we assessed the following variables: 1. Size (cross-sectional area) of the median nerve at the level of the pisiform and hamate bones. To correct for variations in magnification between patient images, size was expressed as the ratio to size at the distal radius. 2. Signal intensity of the median nerve within the carpal tunnel on T2-weighted images. To correct for variations in machine gain on each visit, the values were corrected to the intensity of surrounding fat. 3. Degree of palmar bowing of the flexor retinaculum at the level of the hamate bone as an indirect measure of the volume of the carpal tunnel contents. All images were interpreted in a blinded manner on three separate occasions by two radiologists. Each factor was measured as a continuous variable, and the mean value of the six measurements was used. The coefficient of variation for each factor was 9% to 12%. In addition, each patient underwent nerve conduction studies performed by using standard methods and surface electrodes (15, 16). The peak latency of the sensory and motor action potential of the median and ulnar nerves were recorded. Statistical analysis was performed by using the SPSS software package (SPSS Inc., Chicago, Illinois). The MannWhitney U test was used to compare patients with and those without symptoms of neuropathy, and the Wilcoxon signed-rank test was used for within-group comparisons at baseline and 6 months. Values are expressed as the median (range) with exact P values. P values less than 0.05 were considered statistically significant. The funding source had no role in the collection, analysis, or interpretation of the data or in the decision to submit for publication. Results At presentation, the four patients with the carpal tunnel syndrome had a mean age of 24.8 years (range, 21.5 to 36.3 years) and had had acromegaly for 3.4 years (range, 2.0 to 6.1 years). The five asymptomatic patients had a mean age of 36.5 years (range, 22.0 to 51.2 years) and had had acromegaly for 3.1 years (range, 2.0 to 19 years). Levels of serum growth hormone and IGF-I were 192 ng/mL (range, 26.6 to 250 ng/mL) and 772 ng/mL (range, 144 to 829 ng/mL), respectively, in symptomatic patients and 86 ng/mL (range, 21 to 242 ng/mL) and 728 ng/mL (range, 459 to 823 ng/mL) in asymptomatic patients; the IGF-I levels were elevated in three symptomatic patients and all five asymptomatic patients. After 6 months of treatment, levels of growth hormone and IGF-I levels decreased in all patients (P =0.003 and 0.004, respectively), although levels of IGF-I remained elevated in three of four symptomatic patients and four of five asymptomatic patients. The symptoms of median neuropathy resolved in all four previously symptomatic patients. At presentation, the area of the median nerve at the pisiform bone was significantly larger among patients with symptoms of neuropathy than among those with no symptoms (P =0.014); this difference persisted at 6 months (P =0.027) (Figure 2, top left). The respective median decrease in size was 29% and 5% (P =0.057). These differences were also apparent at the hamate bone (Figure 2, top right), where the nerve decreased in size by 27% in symptomatic patients but only 0.03% in asymptomatic patients (P =0.086). These differences were not due to a generalized nerve hypertrophy; the size of the median nerve at the distal radius was 6.65 mm2 (range, 4.4 to 14.8 mm2) in symptomatic patients compared with 9.06 mm2 (range, 7.4 to 13.9 mm2) in asymptomatic patients. Figure 2. Findings in symptomatic and asymptomatic patients with acromegaly. Top. left right Bottom left. Bottom right. P A similar pattern was observed for T2-signal intensity (Figure 2, bottom left), which decreased by 29% in all four symptomatic patients but increased by 8% in two asymptomatic patients. The two groups did not noticeably differ in the degree of palmar bowing of the flexor retinaculum at presentation or after 6 months of treatment (Figure 2, bottom right). The four symptomatic patients had impaired nerve conduction of both sensory and distal motor action potentials, fulfilling the electrophysiologic criteria for mild carpal tunnel syndrome. Three patients were classified as having moderately severe carpal tunnel syndrome. All of these measurements improved with treatment, although they remained mildly abnormal in all four patients; in contrast, asymptomatic patients experienced minimal change or worsening. At no point was a statistically significant association seen between the decrease in levels of growth hormone and IGF-I and the changes in MRI and electrophysiologic measurements. Discussion We found that clinical symptoms of median neuropathy in acromegaly are associated with an increase in size of the median nerve within the carpal tunnel. These findings are consistent with increased edema of the nerve, which is also supported by the trend toward increased signal intensity on T2-weighted images and the rapid reduction in nerve size and resolution of symptoms that occurred after levels of circulating growth hormone were decreased. However, the chronic impairment of nerve conduction suggests that, as noted in previous reports, this edema must cause some damage to the myelin sheathes (17, 18). The absence of change in bowing of the flexor retinaculum indicates that the overall volume of the carpal tunnel contents did not increase, which contrasts with the MRI findings in idiopathic carpal tunnel syndrome (12). Our findings clarify previous studies of median neuropathy in acromegaly that proposed various pathogenic mechanisms, including an increase in connective tissue within the carpal tunnel (7), demyelination of the Schwann cells (19), bony or synovial overgrowth of the carpal bones (6), or an increase in extracellular fluid within the tunnel itself (8). Our study had limitations. Because the incidence of acromegaly is low (approximately 4 in 1 million persons), our sample was small, making statistical analysis difficult. Although the longitudinal nature of the study meant that each patient acted as his or her own control, study of a simultaneous control group of nonacromegalic patients with idiopathic carpal tunnel syndrome would have enabled us to draw more detailed conclusions about whether the observed mechanisms are specific to acromegaly. The exact role of growth hormone and IGF-I remains uncertain. No statistical correlation was seen between levels of these hormones and radiologic or e

We report three cases of intra‐cardiac metastases from neuroendocrine tumours of the carcinoid type. One presented in a manner identical to a left atrial myxoma; in one patient a left atrial mass was noted during investigations for weight loss and a lung mass; and in the third, two right ventricular deposits were detected on echocardiography when a patient with a disseminated GHRH‐secreting tumour was investigated for dyspnoea. Although to our knowledge this is only the third report of these lesions, we believe that this represents a form of carcinoid heart disease that is distinct from the valvular abnormalities seen in some patients with carcinoid syndrome. Neuroendocrine metastases should be considered in the differential diagnosis of intra‐cardiac tumours.

PURPOSE To show the magnetic resonance (MR) imaging patterns of prolapse and to correlate them with symptoms in patients with constipation or fecal incontinence. MATERIALS AND METHODS Thirty women underwent MR imaging with fast spoiled gradient-recalled acquisition in the steady state. The women were divided into three groups: 10 were asymptomatic volunteers, 10 had constipation, and 10 had fecal incontinence. Visceral prolapse and the configuration of the pelvic floor muscles were identified at rest and during straining. Visceral descent was compared between the three groups. RESULTS Visceral prolapse was seen at multiple sites, most frequently in constipated patients. There was significantly greater bladder base descent (P < .01), uterocervical descent (P < .001), and puborectalis muscle ballooning (P < .05) in the group of constipated patients when compared with the group with fecal incontinence or the asymptomatic group. The degree of anorectal junction descent was significantly greater (P < .05) in the group of incontinent patients when compared with the asymptomatic group. CONCLUSION MR imaging clearly shows pelvic visceral prolapse and pelvic floor configuration on straining. Prolapse frequently involves multiple sites in constipated patients, which is suggestive of global pelvic floor weakness. In contrast, the weakness is frequently posterior in fecally incontinent patients.

The objective of this study was to determine whether magnetic resonance imaging (MRI) could reliably demonstrate fistulas and any associated mass and to see whether these findings were beneficial in the management of the fistula. Twelve consecutive patients presenting with suspected vaginal fistulas were examined prospectively with MRI, using a combination of sequences, for the presence, extent and configuration of fistulas and any associated mass. Comparison was made with CT when available. All patients underwent examination under anesthesia (EUA) and the findings compared. Of the 12 women presenting, seven had vesico-vaginal fistulas (VVF) and seven had recto-vaginal fistulas (RVF). Four women had both types of fistulas. The underlying pathology was cervical cancer (seven cases), colonic cancer (three cases), breast cancer (one case) and ovarian cancer (one case). Vaginal fistulas were unequivocally seen on MRI in eight of 10 cases with fistulas. In the two cases with a difference between the MRI and EUA findings, the MRI was interpreted as showing more than was found at EUA, In the seven women with VVF, MRI detected five of the cases. In the seven women with RVF, MRI detected all seven cases. Magnetic resonance imaging was correct in determining the presence of recurrent disease in the pelvis when an associated mass was seen (seven cases). Computer-assisted tomography was compared in 10 cases and in six eases, the results were comparable and in four cases, more information was obtained from the MRI. Magnetic resonance imaging appears to be accurate in detecting and defining complex gynecologic fistulas and should be considered the investigation of choice to aid the planning of restorative, salvage or palliative surgery.

OBJECTIVE. The aim of this study was to determine the accuracy of MR imaging in revealing complex vaginal fistulas.SUBJECTS AND METHODS. Fifteen patients with clinical symptoms of vaginal fistulas were examined with MR imaging, using a combination of T1-weighted, T2-weighted, and fast multiplanar inversion recovery sequences in the axial plane, along with T2-weighted and fast multiplanar inversion recovery sequences in the sagittal plane. Observers examined the scans for a fistula and any associated masses or collections. The MR findings were recorded with the observers unaware of the results of cystoscopy and sigmoidoscopy under anesthesia. The MR findings were correlated with examination under anesthesia.RESULTS. Vaginal fistulas were seen in ten patients. All fistulas were confirmed surgically. Of the five patients with no fistulas revealed on MR imaging, examination under anesthesia also revealed no fistulas in four. However, in the fifth patient, examination under anesthesia revealed an epithelialized track, which was not seen on MR imaging.CONCLUSION. MR imaging was accurate in revealing and delineating the extent of vaginal fistulas in patients with clinical symptoms of such fistulas.

Pediatria Polska The editor and his board are to be congratulated for producing this new volume (with some help from a Western sponsor) of the journal of the Polish Paediatric Association after a long absence due to the difficult economic conditions in which eastern Europe finds itself today. The quality of the production and the variety and substance of the papers augurs well for the future of Polish paediatrics. The volume of 100 pages contains a number of original papers (alas some submitted as long ago as two to three years), a handful of interesting case reports, a couple of reviews dealing with the use of corticosteroids in allergic disorders and the significance of virus infections in the pathogenesis of asthma respectively, and finally the journal ends with a report of an international meeting on the 'Rights of Children' and a brief historical summary of the development of oncological services for children in Poland. The British paediatrician would not find a great deal to interest him/her-most of the articles are 'common or garden' stuff here. Possibly the best paper came from a dental faculty in Lublin, eastern Poland and dealt with the development of dental caries in insulin dependent diabetic children and controls, and which concluded that there were no significant differences in dentition in the two groups. Surprisingly, many references are from English speaking countries, but regretfully most are outdated and from publications that are used in meeting sponsorships in the West. The attempts at brief summaries of the papers in the English language are, to put it charitably-awful and grossly inaccurate. It might be wise for the editors to consider writing in good English a detailed resume of one or two papers which they think may be of interest to the English speaking readers and confine the other submissions to English titles only. Obviously this journal has taken first brave steps and has a long way to go in order to catch up with the publications in the West. Nonetheless, it was heartening to see so many submissions from various parts of Poland-a clear sign that the editors will not be short of clinical material in the future. J A KUZEMKO

infants and young children with acute febrile mucocutaneous lymph node syndrome..J Pediatr 1975;86:892-8. 6 Rauch AM. Kawasaki syndrome: review of new epidemiologic and laboratory developments. Pediatr Infect Dis J 1987;6:1061-1021. 7 Shulman ST, ed. Kawasaki disease: proceedings of the second international Kawasaki disease symposium. New York: Alan R Liss, 1987:5-72. 8 Fujita Y, Nakamura Y, Sakata K, et al. Kawasaki disease in families. Pediatrics 1989;84:666-9. 9 Kato S, Kimura M, Tsuji K, et al. HLA antigens in Kawasaki disease. Pediatrics 1987;61:252-5. 10 Musada I, Hattori S, Nagata N, et al. HLA antigens in mucocutaneous lymph node syndrome. AmJr Dis Child 1977;131:1417-8. 11 Sasazuki T, Harada F, Kawasaki T. Genetic analysis of Kawasaki disease. In: Shulman S, ed. Kawasaki disease. New York: Alan R Liss, 1987:251-5. 12 Ichida F, Fatica NS, O'Loughlin JE, et al. Epidemiologic aspect of Kawasaki disease in a Manhattan hospital. Pediatrics 1989;84:235-41. 13 Dillon MJD, Hall S. Epidemiology of Kawasaki disease in the UK. Proceedings of the third international Kawasaki disease symposium. Tokyo, 1988:48-51. 14 Hamashima Y, Kishi K, Tasaka K. Rickettsia-like bodies in infantile acute febrile mucocutaneous lymph-node syndrome. Lancet 1973;ii:42. 15 Patriarca PA, Rogers MF, Morens DM, Schonberger LB, Kaminski RM. Kawasaki syndrome: association with the application of rug shampoo. Lancet 1982;ii:578-80. 16 Rogers MF, Kochel RL, Hurwitz ES, Jillson CA, Hanrahan JP, Schonberger LB. Kawasaki syndrome: is exposure to rug shampoo important? AmJ Dis Child 1985;139:777-9. 17 Kato H, Fujimoto T, Inoue 0, et al. Variant strain of Propionibacterium acnes: a clue to the aetiology of Kawasaki disease. Lancet 1983;iu: 1383-7. 18 Tomita S, Kato H, Fujimoto T, Inoue 0, Koga Y, Kuriya N. Cytopathogenic protein in filtrates from cultures of propionibacterium acnes isolated from patients with Kawasaki disease. BMJ 1987;295:229-32. 19 Marrack P, Kappler J. The staphylococcal enterotoxins and their relatives. Science 1990;248:705-1 1. 20 Shulman ST, Rowley AH. Does Kawasaki disease have a retroviral aetiology? Lancet 1986;ii:545-6. 21 Burns JC, Geha RS, Schneeberger EE, et al. Polymerase activity in lymphocyte culture supernatants from patients with Kawasaki disease. Nature 1986;323:814-6. 22 Melish ME, Marchette NJ, Kaplan JC, Kihara S, Ching D, Ho DD. Absence of significant RNA dependent DNA polymerase in lymphocytes from patients with Kawasaki syndrome. Nature 1989;337:288-90. 23 Fujiwara H, Hamashima Y. Pathology of the heart in Kawasaki disease. Pediatrics 1987;61:100-7. 24 Leung DY, Chu ET, Wood N, Grady S, Meade R, Geha RS. Immunoregulatory T cell abnormalities in mucocutaneous lymph node syndrome. J Immunol 1983;130:2002-4. 25 Mason WH, Jordan SC, Sakai R, Takahashi M, Bernstein B. Circulating immune complexes in Kawasaki syndrome. PediatrInfect Dis 1985;4:48-5 1. 26 Levin M, Holland PC, Nokes TJ, et al. Platelet immune complex interaction in the pathogenesis of Kawasaki disease and childhood polyarteritis. BMJ 1985;290: 1456-60. 27 Furukawa S, Matsubara T, Jujoh K, et al. Peripheral blood monocyte/macrophage and serum tumor necrosis factor in Kawasaki disease. Clin Immunol Immunopathol 1988;42:247-5 1. 28 Maury CPJ, Salo E, Pelkonen P. Circulating interleukin-l,1 in patients with Kawasaki disease. N Engl J Med 1988;319:1670-1. 29 Leung DY, Collins T, Lapierre LA, Geha RS, Pober JS. Immunoglobulin M antibodies present in the acute phase of Kawasaki syndrome lyse cultured vascular endothelial cells stimulated by gamma interferon. J Clin Invest 1986;164:1958-72. 30 Leung DY, Cotran RS, Kurt-Jones E, Burns JC, Newburger JW, Pober JS. Endothelial cell activation and high interleukin-1 secretion in the pathogenesis of acute Kawasaki disease. Lancet 1989;ii: 1298-302. 31 Savage CO, Tizard J, Jayne D, Lockwood CM, Dillon MJ. Antineutrophil cytoplasmic antibodies in Kawasaki disease. Arch Dis Child 1989;64:360-3. 32 Tizard EJ, Baguley E, Hughes GRV, Dillon MJ. Antiendothelial cell antibodies detected by a cellular based ELISA in Kawasaki disease. Arch Dis Child 1991;66:189-92. 33 Suzuki A, Tizard EJ, Gooch V, Dillon MJ, Haworth SG. Kawasaki disease: echocardiographic features in 91 cases presenting in the United Kingdom. Arch Dis Child 1990;65:1142-6. 34 Pahl E, Ettedgui J, Neches WH, Parks SC. The value of angiography in the follow-up of coronary involvement in mucocutaneous lymph node syndrome (Kawasaki disease). J Am Coll Cardiol 1989;14:1318-25. 35 Tatara K, Kusakawa S, Itoh K, et al. Long-term prognosis of Kawasaki disease patients with coronary artery obstruction. Heart Vessels 1989;5: 47-51. 36 Naoe S, Takahashi K, Masuda H, Tanaka N. Coronary findings post Kawasaki disease in children who died of other causes. In: Shulman ST, ed. Kawasaki disease. New York: Alan R Liss, 1987:341-6. 37 Brecker SJ, Gray HH, Oldershaw PJ. Coronary artery aneurysms and myocardial infarction: adult sequalae of Kawasaki disease? Br Heart J 1988;59:509-12. 38 Rowley AH, Gonzalez-Crussi F, Gidding SS, Duffy EC, Shulman ST. Incomplete Kawasaki disease with coronary artery involvement. J Pediatr 1987;110:409-13. 39 Furusho K, Kamiya T, Nakano H, et al. High-dose intravenous gammaglobulin for Kawasaki disease. Lancet 1984;ii: 1055-8. 40 Newburger JW, Takahashi M, Burns JC, et al. The treatment of Kawasaki syndrome with intravenous gamma globulin. N Engl J Med 1986;315: 341-7. 41 Shulman ST, Bass JL, Bierman F, et al. Management of Kawasaki syndrome: a consensus statement prepared by North American participants of the third international Kawasaki disease symposium, Tokyo, Japan, December, 1988. Pediatr Infect Dis J 1989;8:663-7. 42 Kato H, Ichinose E, Inoue 0, Akagi T. Intracoronary thrombolytic therapy in Kawasaki disease: treatment and prevention of acute myocardial infarction. In: Shulman ST, ed. Kawasaki disease. New York: Alan R Liss, 1987:445-54. 43 Newburger JW, Takahashi M, Beiser AS, et al. A single intravenous infusion of gamma globulin as compared with four infusions in the treatment of acute Kawasaki syndrome. N Engl 7 Med 1991;324:1633-9.

A prospective study over a one year period examined preadmission illness and its treatment, social characteristics and referral patterns, and inpatient illness progression in 1148 children admitted with a primary diagnosis of gastroenteritis. Admissions were predominantly from socially disadvantaged families: 712 (62%) from social classes IV and V. Approximately a quarter were referred with minimal symptoms, only 12 (1%) with moderate to severe dehydration, and eight (less than 1%) with hypernatraemia. One hundred and ninety two of 1101 (17%) had not seen their general practitioner during the acute illness. One third had received no treatment and one third inappropriate antibiotics, antidiarrhoeals, antiemetics, or changes of milk. Gastroenteritis is a less severe illness than formerly but remains a significant cause of paediatric morbidity. Suboptimal treatment is common. Improved local district hospital and community based resources are needed.

British Journal of UrologyVolume 66, Issue 1 p. 99-100 Pelvic Osteochondroma Causing Haematuria R. R. PHILLIPS, Corresponding Author R. R. PHILLIPS Departments of Radiology and Urology. The Middlesex Hospital LondonDepartment of Radiology, Middlesex Hospital, Mortimer Street, London WIN 8AA.Search for more papers by this authorS. H. LEE, S. H. LEE Departments of Radiology and Urology. The Middlesex Hospital LondonSearch for more papers by this authorG. M. FLANNIGAN, G. M. FLANNIGAN Departments of Radiology and Urology. The Middlesex Hospital LondonSearch for more papers by this author R. R. PHILLIPS, Corresponding Author R. R. PHILLIPS Departments of Radiology and Urology. The Middlesex Hospital LondonDepartment of Radiology, Middlesex Hospital, Mortimer Street, London WIN 8AA.Search for more papers by this authorS. H. LEE, S. H. LEE Departments of Radiology and Urology. The Middlesex Hospital LondonSearch for more papers by this authorG. M. FLANNIGAN, G. M. FLANNIGAN Departments of Radiology and Urology. The Middlesex Hospital LondonSearch for more papers by this author First published: July 1990 https://doi.org/10.1111/j.1464-410X.1990.tb14875.xCitations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References Dahlin, D. C. (1986). Osteochondroma. In Bone Tumours, ed. D. C. Dahlin and K. K. Unni. Fourth edition, Springfield: Thomas. Citing Literature Volume66, Issue1July 1990Pages 99-100 ReferencesRelatedInformation

hours. On no occasion was there more than a temporary improvement in Po2, while the disturbance to the infant during the manipulation required to place the endotracheal tube was considerable. In particular, passage of the endotracheal tube into the right main bronchus without occlusion of the right upper lobe was extremely difficult. One of the infants in whom selective intubation was carried out subsequently underwent a thoracotomy, where multiple pleurotomies were performed. Again, improvement was modest and short lived. In four of the five infants, including the infant in whom surgery was performed, spontaneous resolution and recovery occurred subsequently. The fifth infant died of cor pulmonale complicating bronchopulmonary dysplasia after a period of time at home. We feel that selective bronchial intubation has a place in the management of pulmonary interstitial emphysema but that any improvement may be limited. In particular, improvement may fail to occur when pulmonary interstitial emphysema is associated with bronchopulmonary dysplasia, rather than as a complication of the idiopathic respiratory distress syndrome. The radiological distinction between these two is not always possible.

Journal Article AUDIO‐TAPE/SLIDE TEACHING AIDS Get access R. R. PHILLIPS R. R. PHILLIPS Department of Medical Illustration, Institute of Dermatology, London, W.C.2 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 83, Issue 4, 1 October 1970, Pages 504–505, https://doi.org/10.1111/j.1365-2133.1970.tb15087.x Published: 01 October 1970

Journal Article AN AUDIO‐VISUAL TEACHING UNIT FOR DERMATOLOGY Get access R. R. PHILLIPS R. R. PHILLIPS Department of Medical Illustration, Institute of Dermatology, Lisle Street, London, W.C.2 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 80, Issue 6, 1 June 1968, Page 406, https://doi.org/10.1111/j.1365-2133.1968.tb12327.x Published: 01 June 1968 Article history Accepted: 06 February 1968 Published: 01 June 1968