524
the efficacy of enuresis alarms, reported an overall initial success rate of 68%. However, the range in cures varied from 15 to 100%. Part of this wide variation might be due to difficulties with definition and the lack of universally acceptable criteria of efficacy. These factors hinder comparison of results, so the newly published working definitions for alarm therapy8 are especially welcome. Before a trial of alarm therapy is initiated, baseline data must be recorded-eg, age and sex of the child, severity of the bed-wetting, and presence of other factors that might influence outcome including daytime wetting and organic disease. A 1-month baseline observation period will confirm enuresis severity. Moreover, with supervision, many children achieve continence during this time.9 Initial success should be measured in terms of 14 consecutive dry nights. Alarm treatment usually works in 5-8 weeks; there is little advantage in continuing therapy for more than 2 weeks after initial success. Persistence with an alarm after 16 weeks is unlikely to be beneficial. Drop-outs should be monitored closely and reasons for cessation of therapy noted. Most cases of failure to attend are probably due to treatment failure, although some parents do not keep follow-up appointments because the child has become dry .10 It is harder to define relapse; Butler, in his review of sixteen centres, noted ten definitions. Relapse depends on quantification of three factors: (a) duration of monitoring (most relapses occur within 6 months of treatment); (b) duration over which wet nights are observed; and (c) number of wet nights. By use of these criteria, relapse is defmed as 2 or more wet nights over 2 weeks, and continued success as no relapse in 6 months after initial success. Complete success means that the child is dry 2 years after the initial arrest of
wetting. What factors influence outcome? There are equal for the commonly used pad and bell and body worn alarms, so alarm type is not a factor.An enthusiastic clinic with close monitoring of therapy is important;1112 failures are common if supervision is poor. 13 Failure to respond to the alarm has been explained by domestic difficulties such as sharing a bed, inadequate parental supervision, the child’s lack of interest, and failing to wake to the alarm. These problems should be explored by the therapist because some can be solved-eg, an alarm booster will make the alarm more audible. Adverse environmental success rates
factors, including unsatisfactory housing and family stress, militate against a successful outcome; in the child, behavioural deviance, developmental delay, urological disorder, and daytime wetting are other unfavourable variables.9,14 A child without adverse factors has an excellent chance of achieving dryness. There are few complications of alarm treatment; modem reliable alarms seldom induce buzzer ulcers. Even though relapse after use of an alarm is less
frequent than after pharmacotherapy, careful supervision is necessary for 6 months after treatment. If relapse occurs, treatment may be repeated and the likelihood of success is similar
to
the initial
course
of
therapy. J, Peckham C. Nocturnal enuresis in childhood. Dev Med Child Neurol 1976; 18: 577-89. Douglas JWB. Early disturbing events and later enuresis. In: Kolvin I, Mac Keith RC, Meadow SR, eds. Bladder control and enuresis. Clinics in developmental medicine no 48/49. Philadelphia: Lippincott, 1973. 109-17. Foxman B, Valdez RB, Brook RH. Childhood enuresis: prevalence, perceived impact and prescribed treatments. Pediatrics 1986; 77: 482-87. de Jonge GA. Epidemiology of enuresis: a survey of the literature. In: Kolvin I, Mac Keith RC, Meadow SR, eds. Bladder control and enuresis. Clinics in developmental medicine no. 48/49. Philadelphia Lippincott, 1973: 39-46. Kolvin I, Taunch J, Currah J, et al. Enuresis: a descriptive analysis and a controlled trial. Dev Med Child Neural 1972; 14: 715-26. Wille S. Comparison of desmopressin and enuresis alarm for enuresis. Arch Dis Child 1986; 61: 30-33. Forsythe WI, Butler RJ. Fifty years of enuretic alarms. Arch Dis Child 1989; 64: 879-85. Butler RJ. Establishment of working definitions in nocturnal enuresis. Arch Dis Child 1991; 66: 267-71. Devlin JB, O’ Cathain C. Predicting treatment outcome in nocturnal enuresis. Arch Dis Child 1990; 65: 1158-61. Young GC, Morgan RTT. Reasons for appointment failure among enuretic patients. Common Med 1972; 129: 23-25. Meadow R. How to use buzzer alarms to cure bed-wetting. Br MedJ 1977; ii: 1073-75. Butler RJ. Nocturnal enuresis: psychological perspectives. Bristol: John Wright. 1987. Close GC. Nocturnal enuresis and the buzzer alarm: role of the general practitioner. Br Med J 1980; 281: 483-84. Dische S, Yule W, Corbett J, Hand D. Childhood nocturnal enuresis: factors associated with outcome of treatment with an enuresis alarm. Dev Med Child Neurol 1983; 25: 67-80.
1. Essen
2.
3.
4.
5. 6. 7.
8. 9. 10. 11. 12. 13.
14.
Postoperative pain relief and non-opioid analgesics Routine management of pain after surgery is unsatisfactory and has not advanced substantially for many years.1 Studies published in the past 2 years have shown that about 40% of patients who receive conventional treatment complain of insufficient analgesia and moderate or severe pain. 2,3 After major surgery, an opioid is usually administered "as intramuscularly required". In practice, because of fears among nursing and medical staff about the potential for addiction and depression of ventilation, and because administration of a controlled drug may be inconvenient, opioids are often withheld until the patient is in great discomfort. Moreover, an intramuscular injection given at this time will not bring rapid relief.1 Epidural or intravenous opioids give more continuous analgesia, but at greater risk of ventilatory depression because of the wide variation in individual dose requirements. Patient-controlled analgesia is effective but requires expensive
equipment. Opioids are generally unsuitable for acute pain after day-case surgery because of their sedative action, and may
cause
unnecessary
side-effects when
525
administered to inpatients who have undergone similar procedures. Non-opioid analgesics have been studied extensively in the postoperative period, but their potential contribution as the sole analgesic after minor or intermediate surgery, or as a means of
decreasing, abbreviating, or eliminating opioid requirements after major surgery, is often overlooked. Rectal indomethacin reduces the requirement for morphine, and improves pain relief by comparison with morphine alone, after major abdominal4 or Intravenous thoracics surgery. preoperative administration of indomethacin, followed by 8-hourly suppositories, reduces opioid requirement by 29% by comparison with placebo after abdominal hysterectomy.6Intravenous infusion of lysine acetyl salicylate is as effective as an infusion of morphine after thoracotomy, although it provides poor analgesia when given in bolus doses.8 Rectal ibuprofen, administered regularly, reduces morphine consumption by 19% after gynaecological surgery.9 In a placebo-controlled study10 intramuscular diclofenac reduced morphine requirement by 35 % in patients who had undergone major abdominal In a similar study/1 continuous surgery. 7
adminsitration of ketorolac,
non-steroidal which can be given anti-inflammatory drug (NSAID) intravenously, reduced morphine consumption and pain scores during the first 24 hours after abdominal surgery. Intermittent intramuscular injection of ketorolac is less effective than morphine on the first postoperative day12,13 but appears to provide satisfactory analgesia later, presumably because pain is less intense.12,14 Nefopam, a centrally acting nonopioid analgesic which is not an NSAID, does not share their side-effects. In one study /5 its administration reduced morphine requirements by 30% after abdominal surgery, but in another diclofenac was found to be significantly better than nefopam in its morphine-sparing effect.16 a
new
potential advantages of reduced opioid consumption after major surgery include a lower risk of ventilatory depression or obstruction, improved cooperation and mobility because of reduced sedation, and more rapid restoration of bowel function. Moreover, the many non-opioid analgesics have a long half-life, with less risk of break-through pain. There seems to be little reduction in the frequency of nausea or vomiting. The side-effects of the NSAIDs are well known, and include gastric ulceration, impaired coagulation, and reduced renal function. Gastrointestinal bleeding is rare after short-term administration provided contraindications to the use The
of these agents
are
observedY All NSAIDs inhibit
platelet aggregation by blocking prostaglandin synthetase. Increased blood loss has been reported
during gynaecological surgery when indomethacin 0 - 8 mg/kg had been given preoperatively,6 but not after indomethacin 25 mg
bleeding
or diclofenac.18 The increase in time with ketorolac is not clinically
significant, and there is no interaction with low-dose subcutaneous heparin.19 NSAIDs have not been associated with increased risk of postoperative haemorrhage, although these drugs should be used cautiously in patients with haemostatic abnormalities.19 Renal complications are related also to inhibition of prostaglandin synthesis. Prostaglandins E2, D2, and 12 are potent vasodilators, and in patients with increased concentrations of vasoconstrictor substances such as angiotensin II, or antidiuretic noradrenaline, hormone, administration of NSAIDs may lead to renal vasoconstriction and impaired renal function. 20 Consequently, their use postoperatively may be contraindicated in patients with congestive cardiac failure, hypovolaemia, or hepatic cirrhosis with ascites. Since potassium excretion is impaired by NSAIDs, close monitoring of serum potassium concentrations may be necessary. Nefopam has sympathomimetic and muscarinic side-effects so may be contraindicated in patients with myocardial ischaemia. NSAIDs may be especially beneficial in minor and intermediate surgery; several studies have shown that they provide pain relief that is equal to or better than that of opioids. 21-25 They are valuable after day surgery because they do not cause sedation. The frequency of side effects with the newer agents, diclofenac and ketorolac, is very low. Use of these drugs should reduce opioid requirements, thereby decreasing the frequency of opioid-induced side-effects throughout the postoperative period. 1. Commission on the Provision of Surgical Services. Report of the working party on pain after surgery. London: the Royal College of Surgeons of England, the College of Anaesthetists, 1990. 2. Seers K. Patients’ perception of acute pain. In: Wilson-Barnett J, Robinson S, eds. Directions in nursing research. London: Scutari, 1989: 107-16. 3. Owen H, McMillan V, Rogowski D. Prospective pain therapy: a survey of patients’ expectations and their experiences. Pain 1990; 41: 303-07. 4. Reasbeck PG, Rice ML, Reasbeck JC. Double-blind controlled trial of indomethacin as an adjunct to narcotic analgesia after major abdominal surgery. Lancet 1982; ii: 115-18. 5. Pavy T, Medley C, Murphy DF. Effect of indomethacin on pain relief after thoracotomy. Br J Anaesth 1990; 65: 624-27. 6. Engel C, Lund B, Kristensen S S, Axel C, Nielsen JB. Indomethacin as an analgesic after hysterectomy. Acta Anaesthesiol Scand 1989; 33: 498-501. 7. Jones RM, Cashman JN, Foster JMG, Wedley JR, Adams AP. Comparison of infusions of morphine and lysine acetyl salicylate for the relief of pain following thoracic surgery. Br J Anaesth 1985; 57: 259-63. 8. McAteer E, Dundee JW. Injectable aspirin as a postoperative analgesic. Br J Anaesth 1981; 53: 1069-71. 9. Owen H, Glavin RJ, Shaw NA. Ibuprofen in the management of postoperative pain. Br J Anaesth 1986; 58: 1371-75. 10. Hodsman NBA, Bums J, Blyth A, Kenny GNC, McArdle CS. The morphine sparing effects of diclofenac sodium following abdominal surgery. Anaesthesia 1987; 42: 1005-08. 11. Gillies GWA, Kenny GNC, Bullingham RES, McArdle CS. The morphine sparing effect of ketorolac tromethamine: a study of a new, parenteral non-steroidal anti-inflammatory agent after abdominal surgery. Anaesthesia 1987; 42: 727-31. 12. Power I, Noble DW, Douglas E, Spence AA. Comparison of i.m. ketorolac, trometamol and morphine sulphate for pain relief after cholecystectomy. Br J Anaesth 1990; 65: 448-55. 13. Powell H, Smallman JMB, Morgan M. Comparison of intramuscular ketorolac and morphine in pain control after laparotomy. Anaesthesia 1990; 45: 538-42.
526
14. O’Hara DA, Fragen RJ, Kinzer M, Pemberton D. Ketorolac tromethamine as compared with morphine sulfate for treatment of postoperative pain. Clin Pharmacol Ther 1987; 41: 556-61. 15. McLintock TTC, Kenny GNC, Howie JC, McArdle CS, Lawrie S, Aitken H. Assessment of the analgesic efficacy of nefopam hydrochloride after upper abdominal surgery: a study using patient controlled analgesia. Br J Surg 1988; 75: 779-81. 16. Moffat AC, Kenny GNC, Prentice JW. Postoperative nefopam and diclofenac: evaluation of their morphine-sparing effect after upper abdominal surgery. Anaesthesia 1990; 45: 302-05. 17. Keenan DJM, Cave K, Langdon L, Lea RE. Rectal indomethacin for control of postoperative pain. Br Med J 1984; 288: 240. 18. Rorarius MGF, Baer GA, Metsa-Ketela T, Miralles J, Palomaki E, Vapaatalo H. Effects of peri-operatively administered diclofenac and indomethacin on blood loss, bleeding time and plasma prostanoids in man. Eur J Anaesthesiol 1987; 4: 429-34. 19. Spowart K, Greer TA, McLaren M, Lloyd J, Bullingham RES, Forbes CD. Haemostatic effects of ketorolac with and without concomitant heparin in normal volunteers. Thromb Haemost 1988; 60: 382-86. 20. Orme ML. Non-steroidal anti-inflammatory drugs and the kidney. Br
Med J 1986; 292: 1621-22. 21. Cashman JN, Jones RM, Foster JMG, Adams AP. Comparison of infusions of morphine and lysine acetyl salicylate for the relief of pain after surgery. Br J Anaesth 1985; 57: 255-58. 22. Brown CR, Moodie JE, Evans SA, Clarke PJ, Rotherham BA, Bynum L. Efficacy of intramuscular (IM) ketorolac and meperidine in pain following major oral surgery. Clin Pharmacol Ther 1988; 43: 161. 23. Esteene B, Julien M, Charleux H, Arsac M, Arvis G, Loygue J. Comparison of ketorolac, pentazocine, and placebo in treating postoperative pain. Curr Ther Res 1988; 43: 1173-83. 24. Galasko CSB, Russell S, Lloyd J. Double-blind investigation of multiple oral doses of ketorolac tromethamine compared with dihydrocodeine and placebo. Curr Ther Res 1989; 45: 844-52. 25. McLoughlin C, McKinney MS, Fee JPH, Boules Z. Diclofenac for day-care arthroscopy surgery: comparsion with a standard opioid therapy. Br J Anaesth 1990; 65: 620-23.
When is .
a
fetus
a
dead
baby?
Loss of a pregnancy at any stage after the mother’s awareness and acceptance of it will precipitate a grief reaction. The strength of that reaction is not governed by the gestational age. In Britain, a death in utero is called an abortus before 28 weeks and a stillbirth after 28 weeks. There is a legal obligation to register the stillborn baby with formal documentation to the registrar of births and deaths. The abortus has no such status. To compound this legislative insensitivity it is deemed that "the complete expulsion or extraction from its mother of a product of conception, irrespective of the duration of pregnancy, which breathes or shows other evidence of life"1 for even a few moments must be regarded as a live birth. Such an inconsistency was lately highlighted in an editorial.2 Many of these babies would have been abortuses had they not gasped. This live birth must be recorded with a birth certificate and a death certificate. There are even more troubles for the parents of babies who have received intensive care if, because of lack of intensive care cots, the baby was born in one district and died in another since the birth has to be registered in the district of birth and the death in the district of death. These vagaries extend to the final disposal of the body. There is no legal acceptance of a life in utero before 28 weeks, because the 1929 Infant Life (Preservation) Act presupposes that viability starts at that gestation; viability is now reckoned to begin at least 4 weeks younger. Hence, no formal documentation is
required. The only legal constraints are concerned with the disposal site. The parents have no legal rights over their baby and, until lately, most such babies committed to the hospital incinerator.3 were However, the stillborn baby and any liveborn baby must be buried or cremated. Fortunately, many hospitals now recognise this inconsistency and any member of the medical staff may produce a letter for the parents to take to a funeral director as a formal release certificate so that babies born before 28 weeks may be dealt with according to the parents’ wishes. Slowly the appeals of the grieving parents have been listened to and, thanks to self-help groups such as the Stillbirth and Neonatal Death Society (SANDS)’ and the Miscarriage Association,5it is realised that the abortus must be considered in the same way as the loss of a baby. Nevertheless, the law still does not reflect this attitude. Even the debate last year on abortion with respect to the Human Fertilisation and Embryology Act did not lead to a redefinition of stillbirths, although the allowable limit for termination was reduced to 24 weeks-ie, leaving a 4-week limbo from termination through spontaneous abortion to stillbirth. The published Polkinghome report has added fuel to the fire.The Committee’s intent was to confer a greater respect for the fetus. The stringent recommendation that mothers must sign a form giving blanket agreement to examination of tissues, removal of tissues for research or therapy, and use of the fetus as a teaching aid seems in keeping with the aim, yet one recommendation disallows the mother access to what finally occurs to her baby. There is no doubt that the profession, led by society, more readily accepts that miscarriage, termination, stillbirth, and neonatal death lie in a spectrum of the same grief. These dilemmas and inconsistencies have been addressed by a group from SANDS, who have produced a comprehensive booklet on the subjeCt7 that draws together the practical aspects of baby death and combines them with parental anecdotes which soften and blur legal barriers. Why should the death of a baby be a unique zone of grief? Perhaps it is because to the parents, and to the mother in particular, an unknown potential has been lost. Whatever the reason, surely it is time the law became more sensitive, listened to parents, and shed those artificial barriers of the classification of baby life. 1. International Classification of Diseases. 9th revision. Geneva: World Health Organisation, 1977-78. 2. Editorial. Perinatal mortality rates-time for a change? Lancet 1991; 337: 331. 3. Editorial. Disposal of the previable fetus. Lancet 1988; ii: 611-12. 4. Stillbirth and Neonatal Death Society. 28 Portland Place, London W1N 4DE. 5. Miscarriage Association. PO box 24. Ossett, West Yorkshire WF5 9XG. 6. Review of the Guidance on the Research Use of Fetuses and Fetal Material, July, 1989: presented to Parliament by Command of Her
Majesty. 7. Stillbirth and Neonatal Death neonatal death: guidelines for SANDS at address given in ref
Society. Miscarriage, stillbirth and professionals, 1991 (obtainable from 4).
the efficacy of enuresis alarms, reported an overall initial success rate of 68%. However, the range in cures varied from 15 to 100%. Part of this wide variation might be due to difficulties with definition and the lack of universally acceptable criteria of efficacy. These factors hinder comparison of results, so the newly published working definitions for alarm therapy8 are especially welcome. Before a trial of alarm therapy is initiated, baseline data must be recorded-eg, age and sex of the child, severity of the bed-wetting, and presence of other factors that might influence outcome including daytime wetting and organic disease. A 1-month baseline observation period will confirm enuresis severity. Moreover, with supervision, many children achieve continence during this time.9 Initial success should be measured in terms of 14 consecutive dry nights. Alarm treatment usually works in 5-8 weeks; there is little advantage in continuing therapy for more than 2 weeks after initial success. Persistence with an alarm after 16 weeks is unlikely to be beneficial. Drop-outs should be monitored closely and reasons for cessation of therapy noted. Most cases of failure to attend are probably due to treatment failure, although some parents do not keep follow-up appointments because the child has become dry .10 It is harder to define relapse; Butler, in his review of sixteen centres, noted ten definitions. Relapse depends on quantification of three factors: (a) duration of monitoring (most relapses occur within 6 months of treatment); (b) duration over which wet nights are observed; and (c) number of wet nights. By use of these criteria, relapse is defmed as 2 or more wet nights over 2 weeks, and continued success as no relapse in 6 months after initial success. Complete success means that the child is dry 2 years after the initial arrest of
wetting. What factors influence outcome? There are equal for the commonly used pad and bell and body worn alarms, so alarm type is not a factor.An enthusiastic clinic with close monitoring of therapy is important;1112 failures are common if supervision is poor. 13 Failure to respond to the alarm has been explained by domestic difficulties such as sharing a bed, inadequate parental supervision, the child’s lack of interest, and failing to wake to the alarm. These problems should be explored by the therapist because some can be solved-eg, an alarm booster will make the alarm more audible. Adverse environmental success rates
factors, including unsatisfactory housing and family stress, militate against a successful outcome; in the child, behavioural deviance, developmental delay, urological disorder, and daytime wetting are other unfavourable variables.9,14 A child without adverse factors has an excellent chance of achieving dryness. There are few complications of alarm treatment; modem reliable alarms seldom induce buzzer ulcers. Even though relapse after use of an alarm is less
frequent than after pharmacotherapy, careful supervision is necessary for 6 months after treatment. If relapse occurs, treatment may be repeated and the likelihood of success is similar
to
the initial
course
of
therapy. J, Peckham C. Nocturnal enuresis in childhood. Dev Med Child Neurol 1976; 18: 577-89. Douglas JWB. Early disturbing events and later enuresis. In: Kolvin I, Mac Keith RC, Meadow SR, eds. Bladder control and enuresis. Clinics in developmental medicine no 48/49. Philadelphia: Lippincott, 1973. 109-17. Foxman B, Valdez RB, Brook RH. Childhood enuresis: prevalence, perceived impact and prescribed treatments. Pediatrics 1986; 77: 482-87. de Jonge GA. Epidemiology of enuresis: a survey of the literature. In: Kolvin I, Mac Keith RC, Meadow SR, eds. Bladder control and enuresis. Clinics in developmental medicine no. 48/49. Philadelphia Lippincott, 1973: 39-46. Kolvin I, Taunch J, Currah J, et al. Enuresis: a descriptive analysis and a controlled trial. Dev Med Child Neural 1972; 14: 715-26. Wille S. Comparison of desmopressin and enuresis alarm for enuresis. Arch Dis Child 1986; 61: 30-33. Forsythe WI, Butler RJ. Fifty years of enuretic alarms. Arch Dis Child 1989; 64: 879-85. Butler RJ. Establishment of working definitions in nocturnal enuresis. Arch Dis Child 1991; 66: 267-71. Devlin JB, O’ Cathain C. Predicting treatment outcome in nocturnal enuresis. Arch Dis Child 1990; 65: 1158-61. Young GC, Morgan RTT. Reasons for appointment failure among enuretic patients. Common Med 1972; 129: 23-25. Meadow R. How to use buzzer alarms to cure bed-wetting. Br MedJ 1977; ii: 1073-75. Butler RJ. Nocturnal enuresis: psychological perspectives. Bristol: John Wright. 1987. Close GC. Nocturnal enuresis and the buzzer alarm: role of the general practitioner. Br Med J 1980; 281: 483-84. Dische S, Yule W, Corbett J, Hand D. Childhood nocturnal enuresis: factors associated with outcome of treatment with an enuresis alarm. Dev Med Child Neurol 1983; 25: 67-80.
1. Essen
2.
3.
4.
5. 6. 7.
8. 9. 10. 11. 12. 13.
14.
Postoperative pain relief and non-opioid analgesics Routine management of pain after surgery is unsatisfactory and has not advanced substantially for many years.1 Studies published in the past 2 years have shown that about 40% of patients who receive conventional treatment complain of insufficient analgesia and moderate or severe pain. 2,3 After major surgery, an opioid is usually administered "as intramuscularly required". In practice, because of fears among nursing and medical staff about the potential for addiction and depression of ventilation, and because administration of a controlled drug may be inconvenient, opioids are often withheld until the patient is in great discomfort. Moreover, an intramuscular injection given at this time will not bring rapid relief.1 Epidural or intravenous opioids give more continuous analgesia, but at greater risk of ventilatory depression because of the wide variation in individual dose requirements. Patient-controlled analgesia is effective but requires expensive
equipment. Opioids are generally unsuitable for acute pain after day-case surgery because of their sedative action, and may
cause
unnecessary
side-effects when
525
administered to inpatients who have undergone similar procedures. Non-opioid analgesics have been studied extensively in the postoperative period, but their potential contribution as the sole analgesic after minor or intermediate surgery, or as a means of
decreasing, abbreviating, or eliminating opioid requirements after major surgery, is often overlooked. Rectal indomethacin reduces the requirement for morphine, and improves pain relief by comparison with morphine alone, after major abdominal4 or Intravenous thoracics surgery. preoperative administration of indomethacin, followed by 8-hourly suppositories, reduces opioid requirement by 29% by comparison with placebo after abdominal hysterectomy.6Intravenous infusion of lysine acetyl salicylate is as effective as an infusion of morphine after thoracotomy, although it provides poor analgesia when given in bolus doses.8 Rectal ibuprofen, administered regularly, reduces morphine consumption by 19% after gynaecological surgery.9 In a placebo-controlled study10 intramuscular diclofenac reduced morphine requirement by 35 % in patients who had undergone major abdominal In a similar study/1 continuous surgery. 7
adminsitration of ketorolac,
non-steroidal which can be given anti-inflammatory drug (NSAID) intravenously, reduced morphine consumption and pain scores during the first 24 hours after abdominal surgery. Intermittent intramuscular injection of ketorolac is less effective than morphine on the first postoperative day12,13 but appears to provide satisfactory analgesia later, presumably because pain is less intense.12,14 Nefopam, a centrally acting nonopioid analgesic which is not an NSAID, does not share their side-effects. In one study /5 its administration reduced morphine requirements by 30% after abdominal surgery, but in another diclofenac was found to be significantly better than nefopam in its morphine-sparing effect.16 a
new
potential advantages of reduced opioid consumption after major surgery include a lower risk of ventilatory depression or obstruction, improved cooperation and mobility because of reduced sedation, and more rapid restoration of bowel function. Moreover, the many non-opioid analgesics have a long half-life, with less risk of break-through pain. There seems to be little reduction in the frequency of nausea or vomiting. The side-effects of the NSAIDs are well known, and include gastric ulceration, impaired coagulation, and reduced renal function. Gastrointestinal bleeding is rare after short-term administration provided contraindications to the use The
of these agents
are
observedY All NSAIDs inhibit
platelet aggregation by blocking prostaglandin synthetase. Increased blood loss has been reported
during gynaecological surgery when indomethacin 0 - 8 mg/kg had been given preoperatively,6 but not after indomethacin 25 mg
bleeding
or diclofenac.18 The increase in time with ketorolac is not clinically
significant, and there is no interaction with low-dose subcutaneous heparin.19 NSAIDs have not been associated with increased risk of postoperative haemorrhage, although these drugs should be used cautiously in patients with haemostatic abnormalities.19 Renal complications are related also to inhibition of prostaglandin synthesis. Prostaglandins E2, D2, and 12 are potent vasodilators, and in patients with increased concentrations of vasoconstrictor substances such as angiotensin II, or antidiuretic noradrenaline, hormone, administration of NSAIDs may lead to renal vasoconstriction and impaired renal function. 20 Consequently, their use postoperatively may be contraindicated in patients with congestive cardiac failure, hypovolaemia, or hepatic cirrhosis with ascites. Since potassium excretion is impaired by NSAIDs, close monitoring of serum potassium concentrations may be necessary. Nefopam has sympathomimetic and muscarinic side-effects so may be contraindicated in patients with myocardial ischaemia. NSAIDs may be especially beneficial in minor and intermediate surgery; several studies have shown that they provide pain relief that is equal to or better than that of opioids. 21-25 They are valuable after day surgery because they do not cause sedation. The frequency of side effects with the newer agents, diclofenac and ketorolac, is very low. Use of these drugs should reduce opioid requirements, thereby decreasing the frequency of opioid-induced side-effects throughout the postoperative period. 1. Commission on the Provision of Surgical Services. Report of the working party on pain after surgery. London: the Royal College of Surgeons of England, the College of Anaesthetists, 1990. 2. Seers K. Patients’ perception of acute pain. In: Wilson-Barnett J, Robinson S, eds. Directions in nursing research. London: Scutari, 1989: 107-16. 3. Owen H, McMillan V, Rogowski D. Prospective pain therapy: a survey of patients’ expectations and their experiences. Pain 1990; 41: 303-07. 4. Reasbeck PG, Rice ML, Reasbeck JC. Double-blind controlled trial of indomethacin as an adjunct to narcotic analgesia after major abdominal surgery. Lancet 1982; ii: 115-18. 5. Pavy T, Medley C, Murphy DF. Effect of indomethacin on pain relief after thoracotomy. Br J Anaesth 1990; 65: 624-27. 6. Engel C, Lund B, Kristensen S S, Axel C, Nielsen JB. Indomethacin as an analgesic after hysterectomy. Acta Anaesthesiol Scand 1989; 33: 498-501. 7. Jones RM, Cashman JN, Foster JMG, Wedley JR, Adams AP. Comparison of infusions of morphine and lysine acetyl salicylate for the relief of pain following thoracic surgery. Br J Anaesth 1985; 57: 259-63. 8. McAteer E, Dundee JW. Injectable aspirin as a postoperative analgesic. Br J Anaesth 1981; 53: 1069-71. 9. Owen H, Glavin RJ, Shaw NA. Ibuprofen in the management of postoperative pain. Br J Anaesth 1986; 58: 1371-75. 10. Hodsman NBA, Bums J, Blyth A, Kenny GNC, McArdle CS. The morphine sparing effects of diclofenac sodium following abdominal surgery. Anaesthesia 1987; 42: 1005-08. 11. Gillies GWA, Kenny GNC, Bullingham RES, McArdle CS. The morphine sparing effect of ketorolac tromethamine: a study of a new, parenteral non-steroidal anti-inflammatory agent after abdominal surgery. Anaesthesia 1987; 42: 727-31. 12. Power I, Noble DW, Douglas E, Spence AA. Comparison of i.m. ketorolac, trometamol and morphine sulphate for pain relief after cholecystectomy. Br J Anaesth 1990; 65: 448-55. 13. Powell H, Smallman JMB, Morgan M. Comparison of intramuscular ketorolac and morphine in pain control after laparotomy. Anaesthesia 1990; 45: 538-42.
526
14. O’Hara DA, Fragen RJ, Kinzer M, Pemberton D. Ketorolac tromethamine as compared with morphine sulfate for treatment of postoperative pain. Clin Pharmacol Ther 1987; 41: 556-61. 15. McLintock TTC, Kenny GNC, Howie JC, McArdle CS, Lawrie S, Aitken H. Assessment of the analgesic efficacy of nefopam hydrochloride after upper abdominal surgery: a study using patient controlled analgesia. Br J Surg 1988; 75: 779-81. 16. Moffat AC, Kenny GNC, Prentice JW. Postoperative nefopam and diclofenac: evaluation of their morphine-sparing effect after upper abdominal surgery. Anaesthesia 1990; 45: 302-05. 17. Keenan DJM, Cave K, Langdon L, Lea RE. Rectal indomethacin for control of postoperative pain. Br Med J 1984; 288: 240. 18. Rorarius MGF, Baer GA, Metsa-Ketela T, Miralles J, Palomaki E, Vapaatalo H. Effects of peri-operatively administered diclofenac and indomethacin on blood loss, bleeding time and plasma prostanoids in man. Eur J Anaesthesiol 1987; 4: 429-34. 19. Spowart K, Greer TA, McLaren M, Lloyd J, Bullingham RES, Forbes CD. Haemostatic effects of ketorolac with and without concomitant heparin in normal volunteers. Thromb Haemost 1988; 60: 382-86. 20. Orme ML. Non-steroidal anti-inflammatory drugs and the kidney. Br
Med J 1986; 292: 1621-22. 21. Cashman JN, Jones RM, Foster JMG, Adams AP. Comparison of infusions of morphine and lysine acetyl salicylate for the relief of pain after surgery. Br J Anaesth 1985; 57: 255-58. 22. Brown CR, Moodie JE, Evans SA, Clarke PJ, Rotherham BA, Bynum L. Efficacy of intramuscular (IM) ketorolac and meperidine in pain following major oral surgery. Clin Pharmacol Ther 1988; 43: 161. 23. Esteene B, Julien M, Charleux H, Arsac M, Arvis G, Loygue J. Comparison of ketorolac, pentazocine, and placebo in treating postoperative pain. Curr Ther Res 1988; 43: 1173-83. 24. Galasko CSB, Russell S, Lloyd J. Double-blind investigation of multiple oral doses of ketorolac tromethamine compared with dihydrocodeine and placebo. Curr Ther Res 1989; 45: 844-52. 25. McLoughlin C, McKinney MS, Fee JPH, Boules Z. Diclofenac for day-care arthroscopy surgery: comparsion with a standard opioid therapy. Br J Anaesth 1990; 65: 620-23.
When is .
a
fetus
a
dead
baby?
Loss of a pregnancy at any stage after the mother’s awareness and acceptance of it will precipitate a grief reaction. The strength of that reaction is not governed by the gestational age. In Britain, a death in utero is called an abortus before 28 weeks and a stillbirth after 28 weeks. There is a legal obligation to register the stillborn baby with formal documentation to the registrar of births and deaths. The abortus has no such status. To compound this legislative insensitivity it is deemed that "the complete expulsion or extraction from its mother of a product of conception, irrespective of the duration of pregnancy, which breathes or shows other evidence of life"1 for even a few moments must be regarded as a live birth. Such an inconsistency was lately highlighted in an editorial.2 Many of these babies would have been abortuses had they not gasped. This live birth must be recorded with a birth certificate and a death certificate. There are even more troubles for the parents of babies who have received intensive care if, because of lack of intensive care cots, the baby was born in one district and died in another since the birth has to be registered in the district of birth and the death in the district of death. These vagaries extend to the final disposal of the body. There is no legal acceptance of a life in utero before 28 weeks, because the 1929 Infant Life (Preservation) Act presupposes that viability starts at that gestation; viability is now reckoned to begin at least 4 weeks younger. Hence, no formal documentation is
required. The only legal constraints are concerned with the disposal site. The parents have no legal rights over their baby and, until lately, most such babies committed to the hospital incinerator.3 were However, the stillborn baby and any liveborn baby must be buried or cremated. Fortunately, many hospitals now recognise this inconsistency and any member of the medical staff may produce a letter for the parents to take to a funeral director as a formal release certificate so that babies born before 28 weeks may be dealt with according to the parents’ wishes. Slowly the appeals of the grieving parents have been listened to and, thanks to self-help groups such as the Stillbirth and Neonatal Death Society (SANDS)’ and the Miscarriage Association,5it is realised that the abortus must be considered in the same way as the loss of a baby. Nevertheless, the law still does not reflect this attitude. Even the debate last year on abortion with respect to the Human Fertilisation and Embryology Act did not lead to a redefinition of stillbirths, although the allowable limit for termination was reduced to 24 weeks-ie, leaving a 4-week limbo from termination through spontaneous abortion to stillbirth. The published Polkinghome report has added fuel to the fire.The Committee’s intent was to confer a greater respect for the fetus. The stringent recommendation that mothers must sign a form giving blanket agreement to examination of tissues, removal of tissues for research or therapy, and use of the fetus as a teaching aid seems in keeping with the aim, yet one recommendation disallows the mother access to what finally occurs to her baby. There is no doubt that the profession, led by society, more readily accepts that miscarriage, termination, stillbirth, and neonatal death lie in a spectrum of the same grief. These dilemmas and inconsistencies have been addressed by a group from SANDS, who have produced a comprehensive booklet on the subjeCt7 that draws together the practical aspects of baby death and combines them with parental anecdotes which soften and blur legal barriers. Why should the death of a baby be a unique zone of grief? Perhaps it is because to the parents, and to the mother in particular, an unknown potential has been lost. Whatever the reason, surely it is time the law became more sensitive, listened to parents, and shed those artificial barriers of the classification of baby life. 1. International Classification of Diseases. 9th revision. Geneva: World Health Organisation, 1977-78. 2. Editorial. Perinatal mortality rates-time for a change? Lancet 1991; 337: 331. 3. Editorial. Disposal of the previable fetus. Lancet 1988; ii: 611-12. 4. Stillbirth and Neonatal Death Society. 28 Portland Place, London W1N 4DE. 5. Miscarriage Association. PO box 24. Ossett, West Yorkshire WF5 9XG. 6. Review of the Guidance on the Research Use of Fetuses and Fetal Material, July, 1989: presented to Parliament by Command of Her
Majesty. 7. Stillbirth and Neonatal Death neonatal death: guidelines for SANDS at address given in ref
Society. Miscarriage, stillbirth and professionals, 1991 (obtainable from 4).
