961
EDITORIALS
Oxygen restriction and retinopathy of
prematurity
Neonatologists, now armed to the hilt with continuous monitoring techniques, constantly strive to prevent both hyperoxia and hypoxia in their young patients. Their respectful attitude to the use of supplementary oxygen was acquired as a consequence of bitter lessons learnt from the past-in particular, the epidemic of retinopathy of prematurity (ROP) associated with the routine use of oxygen in the nursery,l and the consequences of restricting the amount of administered oxygen,2a policy adopted in the hope of abolishing ROP. Since universal constraints on supplementary oxygen would be likely to result in hypoxia, which we now appreciate has disastrous consequences for premature infants, it is difficult to understand why such an approach was so readily instituted. However, in 1953 there were 10 000 infants, 7000 in the USA alone, blind from ROP. The positive effect of therapies available at that time (eg, vitamin E3 or corticotropin4) that had been tested before 1953, had not been confirmed in randomised trials, whereas several studies, including a large multicentre trial, had found an association between oxygen restriction and a reduced incidence of ROP.5,6 Thus, in successive years, first the Pediatric Advisory Committee recommended, and then the New York State Department decreed, that because blindness due to retinopathy seemed entirely preventable, oxygen should be administered to infants when clinically indicated, not routinely, and only in a concentration below 40%. Such a conclusion-that a single manoeuvre would abolish ROP-seems naive in the light of our current understanding of the aetiology of the condition. A more critical review of the results of the original studies-on the effects on ROP of oxygen used to prevent cyanosis vs the then routinely used high oxygen concentrations-would have revealed that even drastic oxygen restriction was likely to have only a limited impact. Cases of ROP had occurred in the curtailed oxygen groups, and no concentration of inspired oxygen above room air was unassociated with retinopathy. 5,6 It was subsequently appreciated that ROP was caused by a high arterial rather than inspired oxygen concentration, but use of continuous transcutaneous monitoring to avoid even transient hyperoxia failed to abolish ROP.7 One group8
suggested that the then recommended maximum arterial oxygen tension of 13-3 kPa was too high and that 10 7 kPa should be used. This was achieved by use of a 16% oxygen/84% nitrogen mixture, but only 4 infants were so treated. It is now obvious that the limited impact of oxygen restriction can be explained by the multifactorial aetiology of the condition. Many associations of an increased incidence of ROP have been described, only some which can be explained by a common hyperoxic mechanism. For example, both replacement9 and exchange10 transfusions provide the infant with an increased proportion of adult haemoglobin, with a consequent shift to the right of the oxygen/ haemoglobin saturation curve that improves oxygen delivery to the tissues. Apnoea has also been incriminated, especially if severe enough to require bag and mask resuscitation, but the association remains in infants ventilated by bag and mask with unchanged inspired oxygen concentrations." Disturbances of PaC02 concentrations seem more common in infants who get ROP. 12 Hypercarbia may prevent the protective retinal vasoconstriction response to hyperoxia, but hypocarbia has also been associated with ROP, probably via a different mechanism-vasoconstriction of cerebral blood vessels with consequent diminished retinal blood flow and ischaemia.13 The association of patent ductus arteriosus and ROP is disputed,12,14 but the incidence of ROP is increased in patients with a patent ductus who have been treated with a prostaglandin synthase inhibitor such as indomethacin.15 The retinal vessels and the ductus arteriosus react similarly, by vasoconstriction in response to increased oxygen concentrations, so their response to indomethacin may be similar. Since indomethacin interferes with prostaglandin-mediated effects on vasomotor tone, the drug may impair the vasoconstrictive process that normally protects against the damaging effects of
hyperoxia.16 Many other associations of ROP are less easy to explain by a common hyperoxic aetiology-for example, the damaging effects of bright light on the premature retina, which may or may not be reduced by limiting the standard nursery environmental lighty,18 ROP seems to be increased by certain
complications, diabetes, and adminin the last two weeks of of antihistamines istration pregnancy, but is reduced by toxaemia.19 Results from a small series suggested that only hypoxic antenatal complications increase (roughly double) the risk of retinopathy.20 Retinopathy has even been reported in infants who never received oxygen (term as well as pre-term) and in those with cyanotic congenital heart disease.21 An association between hypoxia and retinopathy has also been claimed and experimental data have been put forward to suggest that the vasoproliferation of retinopathy can be due to local
pregnancy
hypoxia.22 Thus
a
policy
of oxygen restriction would have
a
962
impact on ROP. Moreover, when such a policy was adopted in the 1950s, the impact on both neonatal morbidity and mortality was generally thought to be adverse.23--25 Cross2 suggested that for each case of blindness prevented by oxygen restriction, about 16 infants had died because of inadequate oxygenation. Cross came to this conclusion after reviewing changes in the death rate in limited
both the UK and the USA between 1935 and 1970. He found that, although the rate from days 1 to 6 and in the first 30 min of life had fallen progressively from 1935 in the UK, there was an abrupt hold-up, from about 1950, in the decline in death rate in the remainder of the first day. A similar effect, starting in 1954, was noted in the USA. Several investigators have re-examined the mortality data used by Cross and have reached different conclusions. The calculation of 20 000 unnecessary deaths may have been erroneous because of bias resulting from small differences in the observed and expected values, which were then magnified by the denominator, the number of live births.26 Even the association of the increase in mortality and oxygen restriction has been questioned, because the change in trend in first-day mortality in the UK occurred before Ashton’s report linking oxygen and ROP, and so must have happened before the oxygen restriction policy was implemented.24 Another concern about Cross’ interpretation of the mortality data is that the abrupt halt in the decline of first-day mortality did not occur in isolation but was associated with similar tends in both the stillbirth rate and neonatal mortality.27 Cross maintained that this lack of decline in the stillbirth rate indicated that the change in trend in first-day mortality was real and not caused by reclassification of stillbirths, but the parallel change in neonatal mortality remains to be explained. The adverse trends in mortality and stillbirth rates in the 1950s have subsequently been ascribed to increased activity by both paediatricians and obstetricians in areas where they previously had very little experience, and to their introduction of new treatments and practices that were not always successful and sometimes even deleterious.2g have also influences been Environmental implicated-a rise in exposure to strontium-90 due to testing atomic weapons has been temporally and geographically linked to the excess of deaths.27 Although it is likely that these factors influenced mortality, Cross’ original analysis showed no change in the 1950s in the trend in deaths occurring in the first 30 min of life, and this result goes against any explanation that would implicate a universal influence on mortality at that time. Cross’ hypothesis that oxygen restriction was responsible for the change in trend of first-day mortality accords with the findings of Avery and Oppenheimer. 23 They had suggested that, in the absence of definitive treatment for respiratory distress syndrome, the mortality rate from this disorder
should remain constant. However, they found that the death rate at 30 min to 6 days in infants of birth weight 1-0-2-5 kg had increased from 8% in 1944-1948 to 13% in 1954-1958, and the proportion of necropsies associated with the syndrome rose from 24% to 39% over a similar time. They believed that this increase in death rate was due to oxygen restriction and these observations strengthened the suspicion that, in the oxygen restriction period, some infants with respiratory distress syndrome needed more oxygen than they received. In further support of Cross’ hypothesis, in the USA, where the change in first-day mortality was especially pronounced, the policy of oxygen restriction was adopted before the start of this trend.25 Moreover, the effect was most noticeable in the urban centres such as New York, where such policies would have been expected to have been most effectively and quickly instituted.25 In theory, oxygen restriction should be most harmful in preterm babies, and the New York figures25 tend to bear this out: the adverse trend in death rate was seen in those with low
birthweight. Campbell K. Intensive oxygen therapy as a possible cause of retrolental fibroplasia: a clinical approach. Med J Aust 1951; ii: 48-50. 2. Cross KW. Cost of preventing retrolental fibroplasia? Lancet 1973; ii: 1.
954-56. 3. Owens WC, Owens EU. Retrolental fibroplasia in premature infants: II. Studies on the prophylaxis of the disease: the use of alpha tocopheryl acetate. Am J Ophthalmol 1949; 32: 1631-37. 4. Silverman WA. Retrolental fibroplasia: a modem parable. New York: Grune & Stratton, 1980: 22. 5. Patz A, Hoeck LE, DeLaCruz E. Studies on the effect of oxygen administration in retrolental fibroplasia: I. Nursing observations. Am J Ophthalmol 1952; 35: 1248-52. 6. Kinsey VE, Hemphill FM. Etiology of retrolental fibroplasia and preliminary report of cooperative study of retrolental fibroplasia. Trans Am Acad Ophthalmol Otolaryngol 1955; 55: 15-24. 7. Bancalari E, Flynn J, Goldberg RN, et al. Influence of transcutaneous oxygen monitoring on the incidence of retinopathy of prematurity. Pediatrics 1987; 79: 663-69. 8. MacMahon P, Fleming PJ, Speidel BD, Dunn PM. Low inspired oxygen concentrations in very low birthweight infants needing ventilatory support: an approach to the prevention of retrolental fibroplasia. Br J Obstet Gynaecol 1986; 93: 361-63. 9. Clark C, Gibbs JAH, Maniello R, Outerbridge EW, Aranda JV. Blood transfusion: a possible risk factor in retrolental fibroplasia. Acta Paediatr Scand 1981; 70: 535-39. 10. Yamanouchi I. Successful prevention of retinopathy of prematurity via transcutaneous oxygen monitoring. In: Huch A, Huch R, eds. Continuous transcutaneous blood gas monitoring. New York: Marcel Dekker, 1983: 333. 11. Katzman G, Satish M, Krishnan V, Marcus D, Bovino J. Comparative analysis of lower and higher stage retrolental fibroplasia. Pediatr Res 1982; 16: 294A. 12. Gunn TR, Easdown J, Outerbridge EW, Aranda JV. Risk factors for retrolental fibroplasia. Pediatrics 1980; 65: 1096-100. 13. Shohat M, Reisner SH, Krikler R, Nissenkorn I, Yassur Y, Ben-Sira I. Retinopathy of prematurity: incidence and risk factors. Pediatrics 1983; 72: 159-63. 14. Kingham JD. Retrolental fibroplasia. Acta Fam Pract J 1979; 20: 119-25. 15. Lindemann R, Blystad W, Egge K. Retrolental fibroplasia in premature infants with patent ductus arteriosus treated with indomethacin. Eur J Pediatr 1982; 138: 56-58. 16. Flower RW, Blake DA. Retrolental fibroplasia: evidence for a role of the prostaglandin cascade in the pathogenesis of oxygen-induced retinopathy in the newborn beagle. Pediatr Res 1981; 15: 1293-302. 17. Glass P, Avery GB, Subramanian KNS, Keys MP, Sostek AM, Friendly DS. Effect of bright light in the hospital nursery on the incidence of retinopathy of prematurity. N Engl J Med 1985; 313: 401-04. 18. Ackerman B, Sherwonit E, Williams J. Reduced incidental light exposure: effect on the development of retinopathy of prematurity in low birth weight infants. Pediatrics 1989; 83: 958-62.
963
19. Purohit DM, Ellison RC, Zierler S, Miettinen OS, Nadas AS. Risk factors for retrolental fibroplasia: experience with 3025 premature infants. Pediatrics 1985; 76: 339-44. 20. Johnson L, Schaffer DB, Blessa MI. Factors predisposing to RLF: complications of pregnancy. Pediatr Res 1980; 14: 601. 21. Lucey JF, Dangman B. A re-examination of the role of oxygen in retrolental fibroplasia. Pediatrics 1984; 73: 82-96. 22. Ashton N, Henkind P. Experimental occlusion of retinal arterioles. Br J
Ophthalmol 1965; 49: 225-34. 23. Avery ME, Oppenheimer EG. Recent increase in mortality from hyaline membrane disease. J Pediatr 1960; 57: 553-59. 24. McDonald A. Cerebral palsy in children of very low birth weight. Arch Dis Child 1963; 38: 579-88. 25. Bolton DPG, Cross KW. Further observations on the cost of preventing retrolental fibroplasia. Lancet 1974; i: 445-48. 26. Cohen NM. Cost of preventing retrolental fibroplasia. Lancet 1974; i: 747. 27. Whyte RK. First day neonatal mortality since 1935: re-examination of the Cross hypothesis. Br Med J 1992; 304: 343-46. 28. Editorial. The price of perinatal neglect. Lancet 1974; i: 437-38.
Digit sucking Why do so many children suck their fingers (and even lips, tongue, and inanimate objects)? Perhaps it is simply to provide comfort. Despite a tendency to regard the habit as psychopathologically important, there is little hard evidence: some say that long-term thumb suckers are especially likely to be introverted and emotionally labile.1 Digit sucking habits usually start very early in life-possibly even before birth2 -and are so common that they should be regarded as normal in infancy. About one third of 2t-year-olds suck fingers or thumbs, and another third use artificial comforters.3 Finger sucking is seen in up to 55% of 6-year-olds and 16% of4 11-year-olds but is uncommon in 15-year-olds. Thumb and finger sucking can, in young children, lead to abnormalities in the shape of the dental arches. There are two underlying mechanisms: direct pressure from the digit and reduced intraoral pressure produced by sucking.5 Many people have worried about effects on the facial skeleton from persistent sucking, but recent studies show that, with a few exceptionsit is remarkably difficult to induce permanent distortion of the facial bones.7 Most commonly the digit sucking habit has only a localised effect, resulting in reduction in vertical overlap of the incisor teeth (overbite), often to such a degree that there is a "open bite"-ie, failure of the upper and lower anterior teeth to overlap at all when the posterior teeth are in occlusion. However, in children who persist with finger sucking beyond the age of 8 years there is also a significant increase in protrusion of the incisors.8 The exact effect of a particular habit depends not only on which digit is sucked but also on the manner in which it is placed in the mouth, how much time is devoted to sucking, and the form and behaviour of the lips and tongue both when the digit is in place and when it is out of the mouth. When the habit is given up, the anterior dentoalveolar segments will usually grow into correct occlusal relations unless some other factor such as abnormal tongue or lip activity persists. Even when the habit is abandoned as late as 10 years of age, the
anomaly usually resolves spontaneously.9 Thus, there is little point in worrying about finger sucking until the permanent incisors erupt. Moreover, there are many other causes of a malocclusion, some of which are serious enough to warrant corrective dental
orthodontic treatment. Attempts to stop finger and thumb sucking often fail. Various approaches have been suggested.10,11 For the child who is keen to stop but is unable to do so a simple maxillary orthodontic appliance is usually all that is required, but orthodontists often delay treatment of any persisting habit until the usual age for orthodontic treatment (11-13 years in most patients), because the detrimental effects of sucking can then be corrected mechanically as part of overall treatment. In addition, since children are seldom willing to wear orthodontic appliances for more than 2 years, there is usually little point in prejudicing later cooperation by instituting earlier treatment, especially when most children will give up the habit spontaneously. AH, Piarulle DH. Psychological aspects of prolonged thumb sucking habits. J Clin Orthod 1988; 22: 492-95. 2. Vannerman RA. Digit sucking: It’s time for an attitude adjustment or rationale for the early elimination of digit sucking habits through positive behaviour modification. Int J Oro-Fac Myol 1985; 11: 14-21. 3. Foster TD. A textbook of orthodontics. Blackwell: Oxford, 1975. 4. Buttner M. The frequency of thumb sucking in schoolchildren. Schweiz 1. Geis
Mschr Zahnheil 1969; 97: 580-84. Day AJW, Foster TD. An investigation into the prevalence of molar crossbite and some associated aetiological conditions. Dent Practit 1971; 21: 402-10. 6. Brenchley ML. Is digit sucking of significance? Br Dent J 1991; 171: 5.
357-62. 7. Mills JRE. The effects of orthodontic treatment on the skeletal pattern. Br J Orthod 1978; 5: 133-43. 8. Bowden BD. A longitudinal study of the effects of digit and dummy sucking. Am J Orthod 1966; 52: 887-901. 9. Subtelny JD, Subtelny J. Oral habits: studies in form, function and therapy. Angle Orthod 1973; 43: 347-83. 10. Rincluse DJ, Rincluse DJ. Overcoming finger sucking habits. J Clin Orthod 1986; 20: 46-47. 11 .Van der Linden FPGM, Boersma H. Diagnosis and treatment planning in dento-facial orthopedics. Chicago: Quintessence Publishing, 1987.
Cervical
cancer
screening: quest
for automation
Screening for cervical cancer is a labour-intensive and costly exercise. In the UK alone four million cervical smears are taken annually. Such numbers demand the attention of a large workforce of cytoscreeners, and the productivity of each screener is limited by the need to maintain a high level of vigilance during the screening process so that neoplastic cells are not overlooked. The workload averages 50-80 smears per screener per day. Over the past twenty years large sums of venture capital as well as charitable and government research funds have been invested in projects to automate the screening system. The aim is to increase the volume and speed of throughput of Papanicolaou-stained smears without losing the diagnostic accuracy achieved with the human eye. A fully automated system which can meet these requirements would have enormous commercial potential, especially in
EDITORIALS
Oxygen restriction and retinopathy of
prematurity
Neonatologists, now armed to the hilt with continuous monitoring techniques, constantly strive to prevent both hyperoxia and hypoxia in their young patients. Their respectful attitude to the use of supplementary oxygen was acquired as a consequence of bitter lessons learnt from the past-in particular, the epidemic of retinopathy of prematurity (ROP) associated with the routine use of oxygen in the nursery,l and the consequences of restricting the amount of administered oxygen,2a policy adopted in the hope of abolishing ROP. Since universal constraints on supplementary oxygen would be likely to result in hypoxia, which we now appreciate has disastrous consequences for premature infants, it is difficult to understand why such an approach was so readily instituted. However, in 1953 there were 10 000 infants, 7000 in the USA alone, blind from ROP. The positive effect of therapies available at that time (eg, vitamin E3 or corticotropin4) that had been tested before 1953, had not been confirmed in randomised trials, whereas several studies, including a large multicentre trial, had found an association between oxygen restriction and a reduced incidence of ROP.5,6 Thus, in successive years, first the Pediatric Advisory Committee recommended, and then the New York State Department decreed, that because blindness due to retinopathy seemed entirely preventable, oxygen should be administered to infants when clinically indicated, not routinely, and only in a concentration below 40%. Such a conclusion-that a single manoeuvre would abolish ROP-seems naive in the light of our current understanding of the aetiology of the condition. A more critical review of the results of the original studies-on the effects on ROP of oxygen used to prevent cyanosis vs the then routinely used high oxygen concentrations-would have revealed that even drastic oxygen restriction was likely to have only a limited impact. Cases of ROP had occurred in the curtailed oxygen groups, and no concentration of inspired oxygen above room air was unassociated with retinopathy. 5,6 It was subsequently appreciated that ROP was caused by a high arterial rather than inspired oxygen concentration, but use of continuous transcutaneous monitoring to avoid even transient hyperoxia failed to abolish ROP.7 One group8
suggested that the then recommended maximum arterial oxygen tension of 13-3 kPa was too high and that 10 7 kPa should be used. This was achieved by use of a 16% oxygen/84% nitrogen mixture, but only 4 infants were so treated. It is now obvious that the limited impact of oxygen restriction can be explained by the multifactorial aetiology of the condition. Many associations of an increased incidence of ROP have been described, only some which can be explained by a common hyperoxic mechanism. For example, both replacement9 and exchange10 transfusions provide the infant with an increased proportion of adult haemoglobin, with a consequent shift to the right of the oxygen/ haemoglobin saturation curve that improves oxygen delivery to the tissues. Apnoea has also been incriminated, especially if severe enough to require bag and mask resuscitation, but the association remains in infants ventilated by bag and mask with unchanged inspired oxygen concentrations." Disturbances of PaC02 concentrations seem more common in infants who get ROP. 12 Hypercarbia may prevent the protective retinal vasoconstriction response to hyperoxia, but hypocarbia has also been associated with ROP, probably via a different mechanism-vasoconstriction of cerebral blood vessels with consequent diminished retinal blood flow and ischaemia.13 The association of patent ductus arteriosus and ROP is disputed,12,14 but the incidence of ROP is increased in patients with a patent ductus who have been treated with a prostaglandin synthase inhibitor such as indomethacin.15 The retinal vessels and the ductus arteriosus react similarly, by vasoconstriction in response to increased oxygen concentrations, so their response to indomethacin may be similar. Since indomethacin interferes with prostaglandin-mediated effects on vasomotor tone, the drug may impair the vasoconstrictive process that normally protects against the damaging effects of
hyperoxia.16 Many other associations of ROP are less easy to explain by a common hyperoxic aetiology-for example, the damaging effects of bright light on the premature retina, which may or may not be reduced by limiting the standard nursery environmental lighty,18 ROP seems to be increased by certain
complications, diabetes, and adminin the last two weeks of of antihistamines istration pregnancy, but is reduced by toxaemia.19 Results from a small series suggested that only hypoxic antenatal complications increase (roughly double) the risk of retinopathy.20 Retinopathy has even been reported in infants who never received oxygen (term as well as pre-term) and in those with cyanotic congenital heart disease.21 An association between hypoxia and retinopathy has also been claimed and experimental data have been put forward to suggest that the vasoproliferation of retinopathy can be due to local
pregnancy
hypoxia.22 Thus
a
policy
of oxygen restriction would have
a
962
impact on ROP. Moreover, when such a policy was adopted in the 1950s, the impact on both neonatal morbidity and mortality was generally thought to be adverse.23--25 Cross2 suggested that for each case of blindness prevented by oxygen restriction, about 16 infants had died because of inadequate oxygenation. Cross came to this conclusion after reviewing changes in the death rate in limited
both the UK and the USA between 1935 and 1970. He found that, although the rate from days 1 to 6 and in the first 30 min of life had fallen progressively from 1935 in the UK, there was an abrupt hold-up, from about 1950, in the decline in death rate in the remainder of the first day. A similar effect, starting in 1954, was noted in the USA. Several investigators have re-examined the mortality data used by Cross and have reached different conclusions. The calculation of 20 000 unnecessary deaths may have been erroneous because of bias resulting from small differences in the observed and expected values, which were then magnified by the denominator, the number of live births.26 Even the association of the increase in mortality and oxygen restriction has been questioned, because the change in trend in first-day mortality in the UK occurred before Ashton’s report linking oxygen and ROP, and so must have happened before the oxygen restriction policy was implemented.24 Another concern about Cross’ interpretation of the mortality data is that the abrupt halt in the decline of first-day mortality did not occur in isolation but was associated with similar tends in both the stillbirth rate and neonatal mortality.27 Cross maintained that this lack of decline in the stillbirth rate indicated that the change in trend in first-day mortality was real and not caused by reclassification of stillbirths, but the parallel change in neonatal mortality remains to be explained. The adverse trends in mortality and stillbirth rates in the 1950s have subsequently been ascribed to increased activity by both paediatricians and obstetricians in areas where they previously had very little experience, and to their introduction of new treatments and practices that were not always successful and sometimes even deleterious.2g have also influences been Environmental implicated-a rise in exposure to strontium-90 due to testing atomic weapons has been temporally and geographically linked to the excess of deaths.27 Although it is likely that these factors influenced mortality, Cross’ original analysis showed no change in the 1950s in the trend in deaths occurring in the first 30 min of life, and this result goes against any explanation that would implicate a universal influence on mortality at that time. Cross’ hypothesis that oxygen restriction was responsible for the change in trend of first-day mortality accords with the findings of Avery and Oppenheimer. 23 They had suggested that, in the absence of definitive treatment for respiratory distress syndrome, the mortality rate from this disorder
should remain constant. However, they found that the death rate at 30 min to 6 days in infants of birth weight 1-0-2-5 kg had increased from 8% in 1944-1948 to 13% in 1954-1958, and the proportion of necropsies associated with the syndrome rose from 24% to 39% over a similar time. They believed that this increase in death rate was due to oxygen restriction and these observations strengthened the suspicion that, in the oxygen restriction period, some infants with respiratory distress syndrome needed more oxygen than they received. In further support of Cross’ hypothesis, in the USA, where the change in first-day mortality was especially pronounced, the policy of oxygen restriction was adopted before the start of this trend.25 Moreover, the effect was most noticeable in the urban centres such as New York, where such policies would have been expected to have been most effectively and quickly instituted.25 In theory, oxygen restriction should be most harmful in preterm babies, and the New York figures25 tend to bear this out: the adverse trend in death rate was seen in those with low
birthweight. Campbell K. Intensive oxygen therapy as a possible cause of retrolental fibroplasia: a clinical approach. Med J Aust 1951; ii: 48-50. 2. Cross KW. Cost of preventing retrolental fibroplasia? Lancet 1973; ii: 1.
954-56. 3. Owens WC, Owens EU. Retrolental fibroplasia in premature infants: II. Studies on the prophylaxis of the disease: the use of alpha tocopheryl acetate. Am J Ophthalmol 1949; 32: 1631-37. 4. Silverman WA. Retrolental fibroplasia: a modem parable. New York: Grune & Stratton, 1980: 22. 5. Patz A, Hoeck LE, DeLaCruz E. Studies on the effect of oxygen administration in retrolental fibroplasia: I. Nursing observations. Am J Ophthalmol 1952; 35: 1248-52. 6. Kinsey VE, Hemphill FM. Etiology of retrolental fibroplasia and preliminary report of cooperative study of retrolental fibroplasia. Trans Am Acad Ophthalmol Otolaryngol 1955; 55: 15-24. 7. Bancalari E, Flynn J, Goldberg RN, et al. Influence of transcutaneous oxygen monitoring on the incidence of retinopathy of prematurity. Pediatrics 1987; 79: 663-69. 8. MacMahon P, Fleming PJ, Speidel BD, Dunn PM. Low inspired oxygen concentrations in very low birthweight infants needing ventilatory support: an approach to the prevention of retrolental fibroplasia. Br J Obstet Gynaecol 1986; 93: 361-63. 9. Clark C, Gibbs JAH, Maniello R, Outerbridge EW, Aranda JV. Blood transfusion: a possible risk factor in retrolental fibroplasia. Acta Paediatr Scand 1981; 70: 535-39. 10. Yamanouchi I. Successful prevention of retinopathy of prematurity via transcutaneous oxygen monitoring. In: Huch A, Huch R, eds. Continuous transcutaneous blood gas monitoring. New York: Marcel Dekker, 1983: 333. 11. Katzman G, Satish M, Krishnan V, Marcus D, Bovino J. Comparative analysis of lower and higher stage retrolental fibroplasia. Pediatr Res 1982; 16: 294A. 12. Gunn TR, Easdown J, Outerbridge EW, Aranda JV. Risk factors for retrolental fibroplasia. Pediatrics 1980; 65: 1096-100. 13. Shohat M, Reisner SH, Krikler R, Nissenkorn I, Yassur Y, Ben-Sira I. Retinopathy of prematurity: incidence and risk factors. Pediatrics 1983; 72: 159-63. 14. Kingham JD. Retrolental fibroplasia. Acta Fam Pract J 1979; 20: 119-25. 15. Lindemann R, Blystad W, Egge K. Retrolental fibroplasia in premature infants with patent ductus arteriosus treated with indomethacin. Eur J Pediatr 1982; 138: 56-58. 16. Flower RW, Blake DA. Retrolental fibroplasia: evidence for a role of the prostaglandin cascade in the pathogenesis of oxygen-induced retinopathy in the newborn beagle. Pediatr Res 1981; 15: 1293-302. 17. Glass P, Avery GB, Subramanian KNS, Keys MP, Sostek AM, Friendly DS. Effect of bright light in the hospital nursery on the incidence of retinopathy of prematurity. N Engl J Med 1985; 313: 401-04. 18. Ackerman B, Sherwonit E, Williams J. Reduced incidental light exposure: effect on the development of retinopathy of prematurity in low birth weight infants. Pediatrics 1989; 83: 958-62.
963
19. Purohit DM, Ellison RC, Zierler S, Miettinen OS, Nadas AS. Risk factors for retrolental fibroplasia: experience with 3025 premature infants. Pediatrics 1985; 76: 339-44. 20. Johnson L, Schaffer DB, Blessa MI. Factors predisposing to RLF: complications of pregnancy. Pediatr Res 1980; 14: 601. 21. Lucey JF, Dangman B. A re-examination of the role of oxygen in retrolental fibroplasia. Pediatrics 1984; 73: 82-96. 22. Ashton N, Henkind P. Experimental occlusion of retinal arterioles. Br J
Ophthalmol 1965; 49: 225-34. 23. Avery ME, Oppenheimer EG. Recent increase in mortality from hyaline membrane disease. J Pediatr 1960; 57: 553-59. 24. McDonald A. Cerebral palsy in children of very low birth weight. Arch Dis Child 1963; 38: 579-88. 25. Bolton DPG, Cross KW. Further observations on the cost of preventing retrolental fibroplasia. Lancet 1974; i: 445-48. 26. Cohen NM. Cost of preventing retrolental fibroplasia. Lancet 1974; i: 747. 27. Whyte RK. First day neonatal mortality since 1935: re-examination of the Cross hypothesis. Br Med J 1992; 304: 343-46. 28. Editorial. The price of perinatal neglect. Lancet 1974; i: 437-38.
Digit sucking Why do so many children suck their fingers (and even lips, tongue, and inanimate objects)? Perhaps it is simply to provide comfort. Despite a tendency to regard the habit as psychopathologically important, there is little hard evidence: some say that long-term thumb suckers are especially likely to be introverted and emotionally labile.1 Digit sucking habits usually start very early in life-possibly even before birth2 -and are so common that they should be regarded as normal in infancy. About one third of 2t-year-olds suck fingers or thumbs, and another third use artificial comforters.3 Finger sucking is seen in up to 55% of 6-year-olds and 16% of4 11-year-olds but is uncommon in 15-year-olds. Thumb and finger sucking can, in young children, lead to abnormalities in the shape of the dental arches. There are two underlying mechanisms: direct pressure from the digit and reduced intraoral pressure produced by sucking.5 Many people have worried about effects on the facial skeleton from persistent sucking, but recent studies show that, with a few exceptionsit is remarkably difficult to induce permanent distortion of the facial bones.7 Most commonly the digit sucking habit has only a localised effect, resulting in reduction in vertical overlap of the incisor teeth (overbite), often to such a degree that there is a "open bite"-ie, failure of the upper and lower anterior teeth to overlap at all when the posterior teeth are in occlusion. However, in children who persist with finger sucking beyond the age of 8 years there is also a significant increase in protrusion of the incisors.8 The exact effect of a particular habit depends not only on which digit is sucked but also on the manner in which it is placed in the mouth, how much time is devoted to sucking, and the form and behaviour of the lips and tongue both when the digit is in place and when it is out of the mouth. When the habit is given up, the anterior dentoalveolar segments will usually grow into correct occlusal relations unless some other factor such as abnormal tongue or lip activity persists. Even when the habit is abandoned as late as 10 years of age, the
anomaly usually resolves spontaneously.9 Thus, there is little point in worrying about finger sucking until the permanent incisors erupt. Moreover, there are many other causes of a malocclusion, some of which are serious enough to warrant corrective dental
orthodontic treatment. Attempts to stop finger and thumb sucking often fail. Various approaches have been suggested.10,11 For the child who is keen to stop but is unable to do so a simple maxillary orthodontic appliance is usually all that is required, but orthodontists often delay treatment of any persisting habit until the usual age for orthodontic treatment (11-13 years in most patients), because the detrimental effects of sucking can then be corrected mechanically as part of overall treatment. In addition, since children are seldom willing to wear orthodontic appliances for more than 2 years, there is usually little point in prejudicing later cooperation by instituting earlier treatment, especially when most children will give up the habit spontaneously. AH, Piarulle DH. Psychological aspects of prolonged thumb sucking habits. J Clin Orthod 1988; 22: 492-95. 2. Vannerman RA. Digit sucking: It’s time for an attitude adjustment or rationale for the early elimination of digit sucking habits through positive behaviour modification. Int J Oro-Fac Myol 1985; 11: 14-21. 3. Foster TD. A textbook of orthodontics. Blackwell: Oxford, 1975. 4. Buttner M. The frequency of thumb sucking in schoolchildren. Schweiz 1. Geis
Mschr Zahnheil 1969; 97: 580-84. Day AJW, Foster TD. An investigation into the prevalence of molar crossbite and some associated aetiological conditions. Dent Practit 1971; 21: 402-10. 6. Brenchley ML. Is digit sucking of significance? Br Dent J 1991; 171: 5.
357-62. 7. Mills JRE. The effects of orthodontic treatment on the skeletal pattern. Br J Orthod 1978; 5: 133-43. 8. Bowden BD. A longitudinal study of the effects of digit and dummy sucking. Am J Orthod 1966; 52: 887-901. 9. Subtelny JD, Subtelny J. Oral habits: studies in form, function and therapy. Angle Orthod 1973; 43: 347-83. 10. Rincluse DJ, Rincluse DJ. Overcoming finger sucking habits. J Clin Orthod 1986; 20: 46-47. 11 .Van der Linden FPGM, Boersma H. Diagnosis and treatment planning in dento-facial orthopedics. Chicago: Quintessence Publishing, 1987.
Cervical
cancer
screening: quest
for automation
Screening for cervical cancer is a labour-intensive and costly exercise. In the UK alone four million cervical smears are taken annually. Such numbers demand the attention of a large workforce of cytoscreeners, and the productivity of each screener is limited by the need to maintain a high level of vigilance during the screening process so that neoplastic cells are not overlooked. The workload averages 50-80 smears per screener per day. Over the past twenty years large sums of venture capital as well as charitable and government research funds have been invested in projects to automate the screening system. The aim is to increase the volume and speed of throughput of Papanicolaou-stained smears without losing the diagnostic accuracy achieved with the human eye. A fully automated system which can meet these requirements would have enormous commercial potential, especially in
