INFANTILE BLOODY DIARRHOEA AND COW'S MILK ALLERGY

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Delayed visual maturation was first reported by Illingworth,6 who described two infants, otherwise neurologically normal, who were apparently blind up to 5-6 months of age. They were unable to fixate or follow bright objects and took no notice of their surroundings, despite good pupillary reactions and normal fundi. Evidence of visual function appeared at 6 months and their visual behaviour was normal by 9 months. Illingworth regarded these cases as instances of developmental dissociation. Mellor and Fielder reported four similar cases,7 and were the first to describe the electrophysiological findings in this All their condition. patients had normal the but waveforms of visually electroretinograms, evoked potentials were immature (with normal latency). The evoked potentials became more normal as visual function improved. Others have described similar courses.7-9 Two reports’O," have lately drawn attention to some important features associated with delayed visual maturation: firstly, a high percentage of the infants were either premature or small for gestational age; secondly, many infants with apparently normal overall development showed delay in some specific area at follow-up or exhibited abnormal neurological signs. A review of Illingworth’s and Mellor’s original cases indicated that 2 of their 6 infants had low birthweight, 1 neonatal convulsions, and 1 spasmus nutans. The frequent association with low birthweight and prematurity suggests that a neurological insult in the neonatal period may be a causal factor, and there is some clinical support for this hypothesis. Frequent and detailed neurological assessment by clinical and imaging techniques indicates that perhaps 40% of premature and 2-3% of full-term newborn babies have intracranial haemorrhages, some associated with ventricular dilatation. The neurological signs are often subtle and transient, and the haemorrhage often resolves quickly, but even when the neurological disturbances are mild a high proportion of these infants show delay in visual development as evidenced by the delayed development of visual acuity and maturation of the visually evoked response.IO-12 These infants at follow-up at one year have normal visual and overall development but often show some aberrant neurological signs. Thus, in many ways their clinical 5. Cole GF,

Hungerford J, Jones RB. Delayed visual maturation. Arch Dis Child 1984, 59:

107-10 6. Illingworth RS. Delayed visual maturation. Arch Dis Child 1961; 36: 407-09. 7 Mellor DH, Fielder AR. Dissociated visual development: electrodiagnostic studies

INFANTILE BLOODY DIARRHOEA AND COW’S MILK ALLERGY

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infants who are "slow to see." Dev Med Child Neurol 1980; 22: 327-55. 8. Harel S, Holzman M, Feinsod M. Delayed visual maturation. Arch Dis Child 1983; 58: 298-99 9. Hoyte CS, Jastrzebski G, Marg E. Delayed visual maturation in infancy. Br J 1983; 67: 127-30. 10 Morante A, Dubowitz LMS, Levene M, Dubowitz V. The development of visual function in normal and neurologically abnormal preterm and full term infants. Dev Med Child Neurol 1982; 24: 771-84. 11. Dubowitz LMS, Mushin J, Morante A, Placzek M. The maturation of visual acuity in neurologically normal and abnormal newborn infants. Behav Brain Res 1983, 10: 39-45. 12. Van Hof-Van Dum J, Mohn G, Fetter WPF, Mettau JW, Baerts W. Preferential looking acuity in preterm infants. Behav Brain Res 1983; 10: 47-50.

Ophthalmol

course resembles that in the reported cases of delayed visual development-which strengthens the notion that the delayed visual development is one manifestation of a wider neurological insult.5,9 What might be the mechanism? Disturbances anywhere along the pathway in the retina, optic nerve, mid-brain, or cortex could be responsible. Delay in the development of the macular photoreceptors is an unlikely cause since the infants are blinder than would be expected from abnormal foveal function alone. Delayed myelination has been suggested by Beauvieux,13 who observed a grey discolouration of the optic disc, and by Harel et al,8 who reported prolonged latencies in the evoked potentials. Other observers, who found no such abnormalities, take the view that the condition results from delayed synaptic and in the cortex. dendritic formations visual Electrophysiological evidence favours this hypothesis since the most common abnormality reported is an immaturity of the evoked potential waveform, and maturation of the waveform has been closely correlated with dendritic formation in the visual cortex of premature infants. 14 The theory that cortical dysfunction is the cause of delayed visual maturation receives further support from the fact that in most of the reported cases the infants were of low birthweight and thus prone to hypoxic ischaemic brain injury. Partial ischaemia tends to cause selective neuronal necrosis in the cortex, diencephalon, and mid-brain. The visual cortex, lateral geniculate bodies, and oculomotor nuclei are particularly vulnerable. 15 The evolution of further ingenious tools to study the nervous system and visual function in the newborn should clarify whether the primary lesion is in the cortex or whether there is secondary involvement due to a disturbance further down the visual pathway. Meanwhile, despite reports of neurological normality in some infants with delayed visual maturation, existing data favour the view that this condition is a marker of neurological damage. In most cases an early positive diagnosis can be made by clinical examination and electrodiagnostic tests, and the parents can be reassured of a good prognosis for visual outcome. However, these infants still run a high risk of later neurological troubles and learning disorders, so they should be closely and expertly monitored through childhood.

MANY paediatricians have thought that the vogue for food allergy, if ignored studiously enough, would go away. Not so paediatric gastroenterologists, whose penchant for collecting pieces of gut mucosa has for many years provided the most J. La pseudo-atrophic optique des nouveau nes dysgènesic myelinique des optiques. Ann Oculistique (Paris) 1926, 163: 82-92. 14. Purpura DP. Structure-dysfunction relation in the visual cortex of preterm infants. In: Brazier MAB, Coceani F, eds. Brain dysfunction in infantile febrile convulsions New York. Raven Press, 1976. 223-40. 15. Volpe J Neurology of the newborn. Philadelphia: W. B. Saunders, 1981. 13. Beauvieux voies

1160 concrete

scientific evidence for the existence of food

allergy.

A paper from the late Prof J. T. Harries and his colleagues in London now describes eight infants under the age of two years who presented with bloody, often severe diarrhoea, usually occurring shortly after the introduction of cow’s milk feeds.’ Investigations such as stool culture and microscopy and blood coagulation studies excluded common causes of these symptoms. Colonoscopy revealed macroscopic and microscopic evidence of colitis. The symptoms in all eight patients were protnptly relieved by the removal of all cow’s milk and its products from the diet, a soya-protein-based feed being substituted. Three relapsed 2-6 weeks after starting the soya milk, but the symptoms resolved when this too was withdrawn and a chicken-based feed was substituted. Followup information is not yet available, but three patients who were challenged up to 9 months after diagnosis had such severe relapses that challenge of the other patients was as unjustifiable. Nevertheless, many children with cow’s milk allergy are eventually able to tolerate moderate amounts of cow’s milk,2and the outlook is excellent.3 The observation that bloody diarrhoea in infancy may be due to cow’s milk allergy is not new.4 Endoscopic and histological changes have been noted before.5,6 However, the London workers have provided a new insight by labelling the condition colitis rather than gastrointestinal milk allergy. From a histological and endoscopic standpoint they have contrasted colitis in infancy with the better recognised though different condition of ulcerative colitis which usually occurs in older children. A major difference is that in ulcerative colitis there is little or no evidence of a response to dietary measures.’ Whether the label of colitis, perfectly justifiable as an endoscopic or histological description, is helpful in this - context is questionable. Small-intestinal histological changes in infants with cow’s milk allergy are variable, non-specific, and sometimes absent.’-9 The patients and their families were probably, helped more by the recognition of the allergic basis for the disease than by the application of the rather alarming term colitis, with all its unpleasant connotations. Bloody diarrhoea in infancy due to cow’s milk or soya allergy is probably not uncommon, and not all such patients need expect to see a paediatric gastroenterologist. Guidelines for the management of this and other forms of gastrointestinal cow’s milk allergy have been clearly set out.3 The first step is the suspicion that the symptoms are related to cow’s milk, followed by a complete response to total withdrawal of cow’s milk from the diet. Final confirmation of the diagnosis depends upon the response to a cow’s milk challenge after a period of milk withdrawal. Some less scientifically inclined paediatricians are happy to defer this step, risking treating a child with an inappropriate and difficult form of dietary restriction. But, at some stage, a cow’s milk challenge has to be done, either for confirmation of the diagnosis, or at about the age of 12 months to see if the child has become tolerant of cow’s milk. This challenge carries a risk of a life-threatening

regarded

-

Jenkins HR, Pincott JR, Soothill JF, et al. Food allergy: the major cause of infantile colitis. Arch Dis Child 1984, 59: 326-29. 2. Gerrard JW, Shenassa M. Food allergy: two common types as seen in breast and formula fed babies. Ann Allergy 1983, 50: 375-79. 3. Walker-Smith JA. Gastrointestinal allergy. Practitioner 1978; 220: 562-73. 4. Clein NW. Cow’s milk allergy in infants. Pediatr Clin N Am 1954; 1: 949-62. 5. Lebenthal E. Cow’s milk protein allergy. Pediatr Clin N Am 1975; 22: 827-33. 6. Gryboski JD. Gastrointestinal milk allergy in infants. Pediatrics 1967; 40: 354-62. 7. Savilahti E, Kultunen P, Visakorpi JK. Cow’s milk allergy. In: Lebenthal E, ed. Textbook of gastroenterology and nutrition in infancy. New York: Raven, 1981: 1.

689-708. 8. 9.

Walker-Smith JA. Diseases of the small intestine in children, 2nd ed. Tunbridge Wells: Pitman, 1979; 148-49. Dossetor JFB Soy feeding in infancy. Arch Dis Child 1983; 58: 316.

anaphylactic reaction,3,6,IO,llso all such challenges

must be milk to cow’s reactions Violent adverse hospital. a safe and it is arise after several hours, though challenges may arbitrary policy to keep such children under observation on the ward for 9- 12 hours after the challenge. The services of a dietitian are absolutely essential, for therapeutic failure is sometimes linked to neglect of restriction of foods containing cow’s milk products-not to mention the potential nutritional hazards of elimination diets, especially those involving cow’s milk exclusion.12

done in

MITRAL VALVE SURGERY IN DEVELOPING COUNTRIES IN poor or developing countries prevention is the only long-term answer to rheumatic heart disease.13,14 The means are available, yet there are still many thousands, possibly millions, of young children who have acquired, or who are acquiring, rheumatic heart disease at the moment throughout the world. All clinicians practising in developing countries recognise the importance of prevention but there is a natural desire to help those patients who already have severe rheumatic valvular heart disease, who are mainly young adults and children. Those who offer cardiac surgery must counter arguments that the money could be better spent in other ways; and financial restraints are not the only obstacles they face. The patients are frequently young (of 140 patients who underwent mitral valve surgery in one centre in India, 4 were under the age of ten and 55 were between the ages often and fifteenI5), and the disease is usually severe.16 As well as valvulitis there is often a florid rheumatic myocarditis and pericarditis.17 Furthermore, the choice of the operation is difficult. For pure mitral stenosis most surgeons prefer open mitral valvotomy to a closed operation because it carries a lower risk of embolism during the operation of dislodged thrombi or calcified material, because the subvalvular apparatus can be repaired by separation of fused chordae tendineae, and because the valve can be tested for incompetence at the end of the repair.l8°’9 However, in the Third World closed mitral valvotomy has the advantages of simplicity and cheapness. Expensive heart-lung machines are not needed and the procedure can be done by a general surgeon. In these circumstances echocardiography is a great help since it tells the operator whether the leaflets are pliable and suitable for a valvotomy. In Zaria, Northern Nigeria, closed mitral valvotomy has met with some success in the absence of advanced thoracic surgical facilities.2° However, with complex lesions the 10. Délèze G, Nusslé D. L’mtolerance aux protéines du lait de vache chez l’enfant Helv Paediatr Acta 1975; 30: 135-49. 11. De Peyer E, Walker-Smith J. Cow’s milk intolerance presenting as necrotizing enterocolitis. Helv Paediatr Acta 1977; 32: 509-15. 12. David TJ, Waddington E, Stanton RHJ. Nutritional hazards of elimination diets in children with atopic eczema. Arch Dis Child 1984; 59: 323-25. 13. Agarwal BL. Rheumatic heart disease unabated in developing countries Lancet 1981, ii: 910-11. 14. Editorial. Prevention of rheumatic heart disease. Lancet 1982, i: 143-44. 15. Padmavati S Rheumatic fever and rheumatic heart disease in developing countries. Bull WHO 1978; 56: 543-50. 16. Jaiyesimi F, Anitia Au. Childhood rheumatic heart disease in Nigeria. Trop Geogr Med 1981; 33: 8-13. 17. Silverstein DM, Hansen DP, Ojiambo HP, Griswold HE. Left ventricular function in severe pure mitral stenosis as seen at the Kenyatta National Hospital Am Heart J 1980; 99: 727-33. 18. Bonchek LI. Current status of mitral commissurotomy: indications, techniques and results. Am J Cardiol 1983; 52: 411-15. 19. Kay PH, Belcher P, Dawkins K, Lennox SC Open mitral valvotomy: fourteen years’ experience. Br HeartJ 1983; 50: 4-7. 20. Mabogunje OA, Adesanya CO, Lawrie JH Closed digital commissurotomy for mitral stenosis in Northern Nigeria. Trans Roy Soc Trop Med Hyg 1981, 75: 588-90