2
1310 white-coated juniors, particularly when what is under discussion is the patient’s health and perhaps indeed his life? Attempts to examine the effect of such bedside scenes have not yielded entirely consistent results. Romano,’ using clinical indictors of stress and structured interviews, assessed the effect of bedside teaching rounds at the Peter Bent Brigham Hospital. Although most patients showed little or no signs of anxiety, the need for brief preparatory explanations about the role of teaching rounds was emphasised, together with the need to conduct rounds "tactfully and sympathetically". Kaufman et al2 compared by means of a structured interview the emotional impact of medical and surgical ward rounds. Medical ward rounds were well tolerated, although the jargon annoyed patients, whereas surgical rounds provoked more anxiety because senior surgeons tended to criticise junior house staff in front of the patient. The need for patient preparedness also emerged from a survey carried out by Linfors and Neelon,3 3 who found that bedside case presentations were regarded by patients as a helpful source of education about their illness. In a more extensive study, Wise et all using rating scales and questionnaires, reached a similar conclusion. The seriousness of a patient’s illness or the presence of physiological disturbance did not seem to influence the patient’s perception of the ward round as a necessary part of hospital routine. In a study from Pennsylvania, Simons et als now confirm these findings. 20 patients were admitted to the critical care unit of the University Hospital with suspected myocardial infarction. The following day the patient’s case was presented to a senior physician by a member of the critical care team in the presence of four other members of that team. Stress was assessed by automatic measurement of pulse and blood pressure and by repeated measurements of plasma noradrenaline. In addition, the patients were interviewed and they completed an anxiety questionnaire. Only a small rise in systolic (7 mm Hg) and diastolic (3 mm Hg) blood pressure was observed. Pulse rate and plasma noradrenaline remained unchanged. When questioned, patients reported that bedside presentations were helpful rather than stressful. These results are reassuring as far as they go. The traditional ward round is a universal feature of hospital practice, yet the reassurance needs qualification. Anxiety is a repsonse to uncertainly about what is to happen to an individual. Detailed explanations from staff with time to spend with patients would seem to be an excellent prophylactic. However, it is unsafe to generalise to other situations. Mancia et al in a Milan hospital, used continuous ambulatory monitoring of blood pressure to assess patients’ reactions to their doctor. The pressor response to first measurement of blood pressure is a well-established feature of clinical practice, which is reflected by progressive fall in blood pressure on repeated measurement as patients become familiar with the procedure.’ In Mancia’s study a pressor response and 1. Romano J. Patients’ attitudes and behavior in ward round teaching. JAMA 1941; 117: 664-67. 2 Kaufman MR, Franzblau AN, Kairys D. The emotional impact of ward rounds. J Mount Sinai Hosp 1956, 23: 782-803 3. Linfors ED, Neelon FA. The case for bedside rounds. N Engl J Med 1980; 303: 1230-33. 4. Wise TN, Feldheim D, Mann LS, Boyle E, Rustgi VK Patients reactions to house staff ward rounds. Psychosomatics 1985; 26: 669-72 5. Simons RJ, Baily RG, Zeilis R, Zwillich CW The physiologic and psychological effects of the bedside presentation N Engl J Med 1989, 321: 1273-75. 6 Mancia G, Bertinieri G, Grassi G, et al. Effects of blood pressure measurement by the doctor on patients’ blood pressure and heart rate Lancet 1983; ii. 695-98. 7 Medical Research Council Working Party. MRC trial of treatment of mild hypertension principal results. Br Med J 1985, 291: 97-104 tachycardia were apparent when the doctor approached the patient’s bedside. Maximum rises of 75 mm Hg (systolic) and 36 mm Hg (diastolic) were recorded with an average rise of 26-7/14-9 mm Hg in 48 patients. This "white coat hypertension" reflected a pavlovian response to the doctors’ appearance. An almost identical pressor response was observed when the doctors visited patients on the second occasion. This response differs, therefore, from that observed in the more formal interactions involved in bedside presentation in the Pennsylvanian study. Patients expectations seem to have been different in the two cases. The lesson is simple if something of a cliche—time spent in careful explanation and discussion will set the patient’s mind and his cardiovascular system at rest. SMOKE SCREEN ROUND THE FETUS SMOKING is bad for health-a widely publicised fact and one that is clearly brought to public attention on advertisements and cigarette packets. In the UK, one of the messages from the Health Education Authority also says that cigarette smoking "may cause premature delivery of babies". At antenatal clinics mothers are cautioned, advised, and even castigated to stop smoking if they do smoke, or at least to cut down if they cannot manage to stop altogether, because of the potential dangers to their baby. What are the facts about smoking and pregnancy? Babies born to mothers who smoke are smaller by an average of 200-300 g; delivery is 1-3 days earlier than in normal controls;’ placentas show no significant alteration in sizej23 3 there is placental basement membrane thickening at the vascular syncytial membrane;4 cadmium levels are higher in the placentas of smoking mothers;5 children of smoking mothers have mild behavioural problems;6 and mothers are less likely to get pre-eclamptic toxaemia (PET).7 That these babies are smaller than those born to non-smoking mothers seems of little importance since the difference is generally less than 10% of expected birthweight. Although these babies grow rapidly in their first postnatal year, they still weigh less than the offspring of non-smoking mothers.’ Their lower weight has been attributed to the fact that smokers do not absorb nutrients as readily through their gastrointestinal tracts as do non- smokers ; moreover, smokers tend to eat less and so the baby is malnourished. This may well not be the correct explanation. In a study of babies of truly malnourished wartime mothers from the Netherlands and Leningrad the babies had reduced body fat whereas in a comparison with babies of non-smoking and smoking mothers the fat was identical in amount and distribution. The answer must lie in 1. Pirani BBK Smoking during pregnancy Obstet Gynecol Surv 1978; 33: 1-13. 2. Van der Velde WJ, Treffers PE Smoking in pregnancy the influence on percentile birthweight, mean birthweight, placental weight, menstrual age, perinatal mortality and maternal diastolic blood pressure Gynaecol Obstet Invest 1985, 19: 57-63 3. Mulcahy R, Murphy J, Martin F. Placental changes in maternal weight in smoking and nonsmoking mothers Am J Obstet Gynecol 1970, 106: 703-05 4. Burton GJ, Palmer ME, Dalton KJ Morphometric differences between the placental vasculature of non-smokers, smokers and ex-smokers Br J Obstet Gynaecol 1989, 96: 907-15 5. Kuhnert BR, Kuhnert PM, Debanne S, Williams TG. The relationship between cadmium, zinc, and birth weight in pregnant women who smoke Am J Obstet Gynecol 1987; 157: 1247-51. 6. Harrison R. The use of non-essential drugs, alcohol and cigarettes during pregnancy Irish Med J 1986, 79: 338-41 7. Lehtovita P, Forss M The acute effect of smoking on uteroplacental blood flow in normotensive and hypertensive pregnancy Int J Gynaecol Obstet 1980, 18: 208-11 8. D’Souza SW, Black P, Richards B Smoking in pregnancy associated with skinfold thickness, maternal weight gain, and fetal size at birth. Br Med J 1981, 282: 1661-63

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Page 1: SMOKE SCREEN ROUND THE FETUS

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white-coated juniors, particularly when what is underdiscussion is the patient’s health and perhaps indeed his life?Attempts to examine the effect of such bedside scenes havenot yielded entirely consistent results.Romano,’ using clinical indictors of stress and structured

interviews, assessed the effect of bedside teaching rounds atthe Peter Bent Brigham Hospital. Although most patientsshowed little or no signs of anxiety, the need for briefpreparatory explanations about the role of teaching roundswas emphasised, together with the need to conduct rounds"tactfully and sympathetically". Kaufman et al2 comparedby means of a structured interview the emotional impact ofmedical and surgical ward rounds. Medical ward roundswere well tolerated, although the jargon annoyed patients,whereas surgical rounds provoked more anxiety becausesenior surgeons tended to criticise junior house staff in frontof the patient. The need for patient preparedness alsoemerged from a survey carried out by Linfors and Neelon,3 3who found that bedside case presentations were regarded bypatients as a helpful source of education about their illness.In a more extensive study, Wise et all using rating scales andquestionnaires, reached a similar conclusion. Theseriousness of a patient’s illness or the presence of

physiological disturbance did not seem to influence thepatient’s perception of the ward round as a necessary part ofhospital routine. In a study from Pennsylvania, Simons et alsnow confirm these findings. 20 patients were admitted to thecritical care unit of the University Hospital with suspectedmyocardial infarction. The following day the patient’s casewas presented to a senior physician by a member of thecritical care team in the presence of four other members ofthat team. Stress was assessed by automatic measurement ofpulse and blood pressure and by repeated measurements ofplasma noradrenaline. In addition, the patients were

interviewed and they completed an anxiety questionnaire.Only a small rise in systolic (7 mm Hg) and diastolic(3 mm Hg) blood pressure was observed. Pulse rate andplasma noradrenaline remained unchanged. When

questioned, patients reported that bedside presentationswere helpful rather than stressful.

These results are reassuring as far as they go. Thetraditional ward round is a universal feature of hospitalpractice, yet the reassurance needs qualification. Anxiety is arepsonse to uncertainly about what is to happen to anindividual. Detailed explanations from staff with time tospend with patients would seem to be an excellent

prophylactic. However, it is unsafe to generalise to othersituations. Mancia et al in a Milan hospital, used

continuous ambulatory monitoring of blood pressure toassess patients’ reactions to their doctor. The pressor

response to first measurement of blood pressure is a

well-established feature of clinical practice, which isreflected by progressive fall in blood pressure on repeatedmeasurement as patients become familiar with the

procedure.’ In Mancia’s study a pressor response and

1. Romano J. Patients’ attitudes and behavior in ward round teaching. JAMA 1941; 117:664-67.

2 Kaufman MR, Franzblau AN, Kairys D. The emotional impact of ward rounds.J Mount Sinai Hosp 1956, 23: 782-803

3. Linfors ED, Neelon FA. The case for bedside rounds. N Engl J Med 1980; 303:1230-33.

4. Wise TN, Feldheim D, Mann LS, Boyle E, Rustgi VK Patients reactions to housestaff ward rounds. Psychosomatics 1985; 26: 669-72

5. Simons RJ, Baily RG, Zeilis R, Zwillich CW The physiologic and psychologicaleffects of the bedside presentation N Engl J Med 1989, 321: 1273-75.

6 Mancia G, Bertinieri G, Grassi G, et al. Effects of blood pressure measurement by thedoctor on patients’ blood pressure and heart rate Lancet 1983; ii. 695-98.

7 Medical Research Council Working Party. MRC trial of treatment of mild

hypertension principal results. Br Med J 1985, 291: 97-104

tachycardia were apparent when the doctor approached thepatient’s bedside. Maximum rises of 75 mm Hg (systolic)and 36 mm Hg (diastolic) were recorded with an average riseof 26-7/14-9 mm Hg in 48 patients. This "white coathypertension" reflected a pavlovian response to the doctors’appearance. An almost identical pressor response was

observed when the doctors visited patients on the secondoccasion. This response differs, therefore, from thatobserved in the more formal interactions involved in bedside

presentation in the Pennsylvanian study. Patients

expectations seem to have been different in the two cases.The lesson is simple if something of a cliche—time spent incareful explanation and discussion will set the patient’s mindand his cardiovascular system at rest.

SMOKE SCREEN ROUND THE FETUS

SMOKING is bad for health-a widely publicised fact andone that is clearly brought to public attention on

advertisements and cigarette packets. In the UK, one of themessages from the Health Education Authority also saysthat cigarette smoking "may cause premature delivery ofbabies". At antenatal clinics mothers are cautioned, advised,and even castigated to stop smoking if they do smoke, or atleast to cut down if they cannot manage to stop altogether,because of the potential dangers to their baby.What are the facts about smoking and pregnancy? Babies

born to mothers who smoke are smaller by an average of200-300 g; delivery is 1-3 days earlier than in normal

controls;’ placentas show no significant alteration in sizej23 3there is placental basement membrane thickening at thevascular syncytial membrane;4 cadmium levels are higher inthe placentas of smoking mothers;5 children of smokingmothers have mild behavioural problems;6 and mothers areless likely to get pre-eclamptic toxaemia (PET).7That these babies are smaller than those born to

non-smoking mothers seems of little importance since thedifference is generally less than 10% of expectedbirthweight. Although these babies grow rapidly in theirfirst postnatal year, they still weigh less than the offspring ofnon-smoking mothers.’ Their lower weight has beenattributed to the fact that smokers do not absorb nutrients as

readily through their gastrointestinal tracts as do non-

smokers ; moreover, smokers tend to eat less and so the babyis malnourished. This may well not be the correct

explanation. In a study of babies of truly malnourishedwartime mothers from the Netherlands and Leningrad thebabies had reduced body fat whereas in a comparison withbabies of non-smoking and smoking mothers the fat wasidentical in amount and distribution. The answer must lie in

1. Pirani BBK Smoking during pregnancy Obstet Gynecol Surv 1978; 33: 1-13.2. Van der Velde WJ, Treffers PE Smoking in pregnancy the influence on percentile

birthweight, mean birthweight, placental weight, menstrual age, perinatalmortality and maternal diastolic blood pressure Gynaecol Obstet Invest 1985, 19:57-63

3. Mulcahy R, Murphy J, Martin F. Placental changes in maternal weight in smokingand nonsmoking mothers Am J Obstet Gynecol 1970, 106: 703-05

4. Burton GJ, Palmer ME, Dalton KJ Morphometric differences between the placentalvasculature of non-smokers, smokers and ex-smokers Br J Obstet Gynaecol 1989,96: 907-15

5. Kuhnert BR, Kuhnert PM, Debanne S, Williams TG. The relationship betweencadmium, zinc, and birth weight in pregnant women who smoke Am J ObstetGynecol 1987; 157: 1247-51.

6. Harrison R. The use of non-essential drugs, alcohol and cigarettes during pregnancyIrish Med J 1986, 79: 338-41

7. Lehtovita P, Forss M The acute effect of smoking on uteroplacental blood flow innormotensive and hypertensive pregnancy Int J Gynaecol Obstet 1980, 18: 208-11

8. D’Souza SW, Black P, Richards B Smoking in pregnancy associated with skinfoldthickness, maternal weight gain, and fetal size at birth. Br Med J 1981, 282:1661-63

Page 2: SMOKE SCREEN ROUND THE FETUS

1311

reduction of cell number or cell size. Animal work has

shown that there is a reduction in the cell number in littersfrom rats and pigs exposed to smoking in pregnancy;9,1O thismay also be true in human beings.

It has been suggested that babies of mothers who smokedduring pregnancy are hyperactive and have mild

behavioural problems in childhood.6 Animal work showsthat nicotine has a deleterious effect on the development ofthe rat brain," but since assessment of behavioural activitytends to be subjective and may be influenced by manyfactors, including the personality of the smoking mother,this cannot be a serious argument yet. Moreover, nicotine isonly one of 2000 toxic substances in cigarettes. Prematuredelivery, however, is a fact, but is usually.only by a few days.In babies who are born after 36 weeks, a few days may be oflittle consequence, whereas those who are born before thattime may be put into greater jeopardy by this added

prematurity.Placentas in smoking mothers are usually the same size as

in their non-smoking counterparts. Although malnutritiondoes not seem to explain the smaller fetal size, the lowerbirthweight might be due to the toxic effects of the multipleingredients in cigarette smoke or to changes in placentalperfusion. Burton et al4 have documented thickening of thebasement membrane at the vascular syncytial membrane,but this study does not indicate whether the thickening liesat the basement of the trophoblastic cells or at the basementof the fetal capillaries within the villus; such histologicaldetails might throw some light on the possible aetiology ofthis lesion. Cadmium, which is mentioned as the possiblecausal agent in placental basement membrane thickeningand fetal size reduction,4 is found in relatively high levels inplacental tissue and is low in blood from the umbilicalvessels.s The suggested mode of action is that cadmium

competes with zinc, which is associated with intrauterinegrowth retardation. The controversial nature of theevidence with respect to zinc must in turn cast doubt uponthe cadmium competition theory.The potential of increased congenital malformation of the

fetus has been raised 12 and denied.l3 There is some evidenceof a higher frequency of acute lymphoblastic leukaemia inthe children of mothers who have smoked duringpregnancy,14 but again many factors are implicated in thiscondition. On the plus side for cigarette smoking is the factthat mothers who smoke have less PET than non-smokingmothers.7 However, it is unthinkable that this known toxichabit should be recommended as a protective factor againstPET.The evidence against not smoking in pregnancy is not

clear cut, but the evidence against smoking per se

undoubtedly is. Not only is the smoker at greater risk ofpulmonary, gastrointestinal, and vascular diseases but also

9. Haworth JC, Ford JC The acute effect of smoking on uteroplacental blood flow innormotensive and hypertensive pregnancy. Am J Obstet Gynecol 1972; 112: 653-56

10. Dawes GS. The physiological determinants of fetal growth. J Reprod Fertil 1976, 47:183-87.

11 Lichtensteiger W, Ribary U, Schlumpf M, Odermatt B, Widmer HR. Prenataladverse effects of nicotine on the developing brain. In: Boer JG, Feenstra MGP,Mirmiran M, Swaab DF, Van Haaren F, eds. Progress in brain research, vol 73.Amsterdam: Elsevier, 1988: 137-57

12. Nash NE, Persaud TVN. Embryopathic risks of cigarette smoking Exp Pathol 1988;33: 65-73.

13 Beeley L. Adverse effects of drugs in the first trimester of pregnancy Clin Obstet

Gynaecol 1986, 13: 177-9514. Stjernfeldt M, Berglund K, Lindsten J, Ludvigsson J Maternal smoking during

pregnancy and nsk of childhood cancer Lancet 1986; ii: 1350-52.15. Willers S, Shutz A, Attewell R, Skerfuing S. Relation between lead and cadmium in

blood and the involuntary smoking of children Scand J Work Environ Health 1988;14: 383-89.

the evidence that these conditions are increasing amongpassive smokers must give cause for alarm.15 Althoughcigarette smoking has decreased over the past two decades,there are indications that young women are increasinglytaking up the habit, and these are the people who will bebearing the children of the future and allowing them to lie ina polluted atmosphere of side-stream smoke. Educationabout the dangers of smoking should be delivered by themedical profession at any time; pregnant women comprise acaptive young audience who may be persuaded to stop thehabit and may even be able to persuade those around them todo so. However, this advice is not being delivered, not beingdelivered correctly, or is not being heard.16-18 Is the

approach to the mother wrong? It is dishonest to say there isserious evidence that her fetus is at risk if she does not giveup smoking. Instead health professionals should emphasisethe dangers of smoking to the mother’s own health and thedangers of side-stream smoking to her child, who may getsmoking-related diseases postnatally.

RECURRENT ERYTHEMA MULTIFORME ANDHERPES SIMPLEX VIRUS

ERYTHEMA multiforme (EM) is generally regarded as ahost-specific immune response to a wide variety of antigenicstimuli. The clinical lesions are characteristic, with

erythematous papules acrally distributed evolving intoconcentric target lesions. Although usually mild and

self-limiting, EM may be recurrent or progress to toxicepidermal necrolysis, or there may be severe mucousmembrane involvement (Stevens-Johnson syndrome).Despite its episodic nature, a precipitating agent cannotalways be identified.1 Many classes of drug and numerousinfective agents, of which herpes simplex is perhaps the bestknown, have been incriminated. However, the list ofassociated conditions is long and includes connective tissuediseases such as systemic lupus erythematosus,2 as well asmalignant disorders such as leukaemia and lymphoma.3 EMhas been described after radiotherapy, BCG scarification,and vaccinations including hepatitis B.16 It may be

precipitated by contact with chemicals such as 9-

bromofluorene, terpenes, and even perfumes.7-9 Outbreaksof EM in the luteal phase of the menstrual cycle have beendescribed as a manifestation of autoimmune progesterone

16. Ashford A, Gerlis R, Johnson P. Smoking in pregnancy: is the message gettingthrough? J R Coll Gen Pract 1986, 36: 494-95

17 Williamson DF, Serdula MK, Kendnck JS, Bmkin NJ. Comparing the prevalence ofsmoking in pregnant and nonpregnant women, 1985 to 1986. JAMA 1989; 261:70-74.

18 Hilton CA, Condon JT Changes in smoking and drinking during pregnancy. Aust NZJ Obstet Gynaecol 1989; 29: 18-21.

1. Tonnesen M, Soter N. Erythema multiforme. a clinical review. J Am Acad Dermatol1979; 1: 357-64.

2. Rowell N, Beck S, Anderson J. Lupus erythematosus and erythema multiforme-likelesions. Arch Dermatol 1963; 88: 176-80.

3. Elias P, Fritsch P. Erythema multiforme In: Fitzpatrick T, Eisen A, Wolff K, et al, eds.Dermatology in general medicine. 3rd ed New York: McGraw-Hill, 1987.

4. Nawalka P, Mathur N, Malhotra Y. Severe erythema multiforme (Stevens-Johnsonsyndrome) following telecobalt therapy. Br J Radiol 1972; 45: 768-69.

5 Tscher E, Jessen T, Robertson G, Becker L. Erythema multiforme as a complicationof BCG scarification technique Arch Dermatol 1979; 115: 614-15.

6. Milstien J, Kuritsky J. Erythema multiforme and hepatitis B immunisation. ArchDermatol 1986; 122: 511-12.

7. Defoe C. Erythema multiforme bullosum caused by 9-bromofluorene. Arch Dermatol1966; 94: 545-81

8. Kirby J. Erythema multiforme associated with contact dermatitis to terpenes ContactDermatitis 1978, 4: 238.

9 Thompson J, Wansker B. A case of contact dermatitis, erythema multiforme, and toxicepidermal necrolysis. J Am Acad Dermatol 1981; 5: 666-69.