- Email: [email protected]
CAPTOPRIL EFFECT ON HYPERTENSION IN PATIENT WITH RENIN-PRODUCING TUMOUR
149
acid) were normal, as were chest, abdominal, and skull X-rays. At this stage the patient and her family refused to cooperate and demanded surgical treatment of a presumed insulinoma. A distal pancreatectomy was done, but the pancreas delic
macroscopically and histologically normal. The patient made a good postoperative recovery and her blood-glucose was
remained normal. At this time the results of insulin assays
Barnet General Herts
off
on
A. STELLON N. H. TOWNELL*
Hospital,
*Present address: Academic don NW3 2QG.
Department
of Surgery,
Royal
Free
Regional Respiratory Laboratory,
ster-
T.H. LEE W.M. SEYMOUR
Brook General Hospital, London SE18 4LW
on
admission became available. They were samples In view of this serum-C-peptide levels (see table). very high were measured and found to be suppressed. A search uf the patient’s house then revealed a hidden store of syringes and needles. This case reinforces Scarlett’s opinion that C-peptide levels be measured as an initial investigation in all patients with hypogtycxmia and hyperinsulinism. In our case major surgery would thus have been avoided. sent
ing is symptomatic, and, although our patient was given oids, there is no good evidence to support their efficacy.44
Hospital, Lon-
CAPTOPRIL EFFECT ON HYPERTENSION IN PATIENT WITH RENIN-PRODUCING TUMOUR
SiR,-Primary reninism is a rare syndrome caused by juxtaglomerular cell tumours of the kidneys some Wilms’ tumours,7 and occasionally by other renin-producing neoplasmaWe have seen a case of malignant renin-producing tumour with the full-blown picture or primary reninism, including severe hypertension and secondary aldosteronism. This patient was treated with the angiotensin-i-converting-enzyme inhibitor, captopril (SQ 14225).9 The patient is a 32-year-old woman with one healthy child. She was in perfect health until September, 1975, when hypertension was discovered. Because of poor blood-pressure control with hydrochlorothiazide and propranolol, the patient was
PNEUMONITIS CAUSED BY PETROL SIPHONING
SIR,-Robinson’ has described one hazard of petrol shortages-perioral erythema from siphoning petrol into the mouth. As prices rise and petrol becomes scarce, medical problems due to petrol siphoning may become more common. We have seen a patient with pneumonitis caused in this way. A previously healthy 22-year-old man was siphoning petrol when he sucked about half a cupful into his mouth. He had severe pain in his throat and lost consciousness for a few minutes. He was asymptomatic after this, but thought he had better be seen in the casualty department because of his loss of consciousness. When he was seen, there was a strong smell of petrol but there were no other abnormal signs. However, a chest X-ray showed right-middle-lobe shadowing. His arterial blood gases deteriorated over 4 h from pH 7.32, P02 11 kPa (lkPa=7.5 mm Hg), PC02 4-2 kPa, bicarbonate 15.5 mmol/1, to pH 7.36, POz 5.2 kPa, PC02 4.4 kPa, bicarbonate 18.5 5 mmol/l, despite 1 g methylprednisolone. Over the next 2 days, he needed 40% oxygen to keep his arterial oxygen within the normal range. During this time he coughed up a few specks of blood on one occasion but was otherwise symptom-free and his peak expiratory flow-rate (PEFR) was normal. He was able to maintain a normal PaOz breathing air from the 4th day onwards. However, his chest X-ray showed no change during his week in hospital. Formal respiratory-function tests on the 5th day of his illness were normal and the chest X-ray 1 month later was very much improved. The localised pneumonitis caused by petroleum distillates is thought to be due to aspiration (their low surface tension would facilitate their spread along mucosal surfaces) rather than inhalation of fumes or absorption.23For this reason, many clinicians would be reluctant to subject these patients to gastric lavage or other measures to induce vomiting. However, this man’s pulmonary problems must have been more widespread than the X-ray suggested because his hypoxia seemed incompatible with such a localised abnormality in his middle lobe. The lack of generalised radiological shadowing during his illness would be against an alveolitis, and his normal PEFR would exclude any significant large-airway disease. We suggest that the hypoxia may have been due to a ventilation-perfusion mismatch from bronchiolitis, which resolved over the 4 days, in addition to the more obvious abnormality in the right middle lobe. The treatment for petroleum poison1. Robinson BL. The hazard of petrol shortage. Br Med J 1973; iv: 614. 2. Baldachin BJ, Melmed RN. Clinical and therapeutic aspects of kerosene poisoning:a series of 200 cases. Br Med J 1964; ii: 28-30. 3 Richardson JA, Pratt Thomas HR. Toxic effects of varying doses of kerosene administered by different routes. Am J Med Sci 1951; 221: 531-6.
-1
01
2
3
4
56
Hours
Blood-pressure response to captopril in patient with hypertension due to renin-producing tumour. admitted to hospital in August, 1976. A large pelvic tumour and persistent hypokalaemia were found. After removal of a large tumour (grapefruit sized) adjacent to the normal left ovary, the hypertension and hypokalsemia disappeared. The true nature of the tumour, which was malignant histologically, could not be established. Hypertension and hypokalaemia recurred 9 months later. Investigations suggested primary reninism from recurrent tumour growth. The blood-pressure was 240/130 mm Hg and serum-potassium 3.2 mmol/l. Plasma-renin-activity was 150 ng/ml/h (normal range 03-2.0), plasma-aldosterone 5.0 MI, Chicoine L, Legeve G, Hillman E. Adrenocorticosteroid treatof hydrocarbon pneumonia in children: a cooperative study.J Pediat 1972; 81: 366-9. 5. Robertson PW, Klidjian A, Harding LK, Walters G, Lee MR, Robb-Smith 4. Marks
ment
AHT.
Hypertension
due
to a
renin-secreting
renal
tumor.
Am
J
1967; 43: 963-76. 6. Kihara J, Kitamura S, Hoshimo T, Seida H, Watanabe T. A hitherto
Med
unre-
ported vascular tumour of the kidney: a proposal of "juxtaglomerular cell tumour". Acta Path Jap 1968; 18: 197-206. 7. Mitchell JD, Baxter TJ, Blair-West JR, McCardie DH. Renin levels in nephroblastoma (Wilms’ tumour): report of a renin-secreting tumour. Arch Dis Child 1970; 45: 376-84. 8. Genest J, Rojo Ortega JM, Kuchel O, Boucher R, Nowaczynski W, Lefebvre R, Chretien M, Cantin J, Granger P. Malignant hypertension with hypokalemia in a patient with renin-producing pulmonary carcinoma. Trans Assoc Am Phys 1975; 88: 192-201. 9. Ondetti MA, Rubin B, Cushman DW. Design of specific inhibitors of angiotensin-converting enzyme: new class of orally active antihypertensive agents. Science 1977; 196: 441-4.
150
nmo1/l (0-3-0-8), and urinary aldosterone 300 nmol/day (<56). At angiography the kidneys and the renal arteries were normal. Catheterisation of the cava vena inferior revealed high renin values at all levels. At operation (May, 1978) a large amount of tumour was removed from peritoneum and omentum, as was a big tumour close to the liver. Tumour tissue contained 1-6 Goldblatt units of renin per gram tissue (with reference to the M.R.C. standard). Kidneys from non-renovascular, hypertensive patients contain less than 0.05 units/g, but kidneys from renovascular patients may reach 1 unit/g. After surgery blood-pressure and plasma-renin fell to normal. The patient remained in good condition for about 6 months, when hypertension returned and renin values rose. This time plasma-renin-activity was 80-132 ng/ml/h, and she was readmitted February, 1979. The patient was put on captopril and her blood-pressure responded to 25 and 50 mg (see figure). The blood-pressure fall was dramatic, and on 150 mg three times a day by mouth the patient remained normotensive. Signs of aldosteronism subsided within a week. A new investigation revealed tumour growth close to the liver and at operation in April, 1979, tumour growth was observed in other parts of the abdomen. All visible tumour was removed, but the patient remained hypertensive after this operation. Treatment with captopril 50 mg three times a day has kept blood-pressure normal since then. To our knowledge, this is the first report of the efficacy of captopril in a patient with a renin-producing tumour. The drug was very effective in maintaining normal blood-pressure and serum-potassium without any secondary effects. Departments of Nephrology, Endocrinology, Surgery and Pathology, Sahlgrenska Sjukhuset, S413 45 Göteborg, Sweden, and Department of Medicine, Centrallasarettet, Mölndal
M. AURELL
A. RUDIN L.-E. TISELL L. G. KINDBLOM G. SANDBERG
LOWERING BLOOD-PRESSURE
SIR,-Dr Stewart (April 21, p. 861) claims to have demonstrated that "the relative risk of myocardial infarction in patients with FDP [final diastolic pressure] reduced to <90 mm Hg was more than five times that in patients with FDP 100-109 mm Hg (p<0.01)". He does not state how his statistical analyses were carried out, but the flaw in this study is readily apparent in fig. 1, which shows the frequency distribution of FDPs in 169 patients, 29 of whom had a myocardial infarction and 140 of whom did not. Whatever analysis Stewart used relied heavily on a unimodal distribution of non-myocardial infarction and a bimodal distribution of myocardial infarction. If we take at face value the fact that the myocardial infarction group is truly a bimodal population, then it naturally follows that the incidence of myocardial infarction at the left-hand side of the frequency pressure histogram will be greater in these low-pressure patients. This leads to a statistical problem of comparing bimodal with unimodal populations, a problem which Stewart does not discuss. Moreover, the bimodality of the very small myocardial infarction group is dependent upon the presence of only 3 patients in the 80-85 mm Hg myocardial infarction group. Statisticians would not consider bimodality proved in this group of only 29 patients, and the conclusion that there is an increased incidence of myocardial infarction in the low-pressure group cannot be valid statisti-
cally. Although Stewart claims to have controlled all the risk factors for myocardial infarction in each group, 3 of his 29 myocardial infarction group had hypercholesterolsemia, while only 2 out of 140 non-infarct patients had this feature. Stewart’s conclusions remain only a hypothesis. V. A.
Hospital,
Tucson, Arizona 85723, U.S.A., and Renal Section,
University of Arizona College of Medicine
MURRAY A. KATZ
ONCE-DAILY &bgr;-ADRENOCEPTOR ANTAGONISTS AND ARTERIAL PRESSURE
SIR,-It was with great interest that we read the paper on the influence of once-daily administration of p-adrenoceptor antagonists on arterial pressure and its variability by Dr Watson and colleagues (June 9, p. 1210). That many, if not all, of the available beta blockers have a hypotensive action lasting well beyond 24 h from the time of last administration is substantiated by many non-invasive studies and also by our own study on atenoloP which Watson et al. cite. However, a lack of consistency in the effect on night-time and early-morning blood-pressure (BP) should not be confused with duration of action of the drugs, the former being ascertainable almost exclusively by this form of ambulatory monitoring. We do not feel that the lack of an early-morning effect is a universal feature of beta blockers,2 even when given once daily, since other studies from our unit have shown variable responses.3-5 It is a pity that Watson et al. did not feel able to separate their results according to drug taken. One apparently consistent observation is that groups of patients with higher pretreatment BP (and by inference, necessarily poorer control with monotherapy) show the greatest tendency towards lack of early-morning BP control. The pretreatment data of Watson et al. show a post-waking rise in BP before the patient rises from bed, confirming our results. 6,7 We agree that BP variability is probably important in the mechanism of cardiovascular disease. The validity of using standard deviation (or variance) of a given period of recorded signal in this way is however questionable given the nonstationarity of the dataeven with the partial control of physical activity during their studies. The apparent gaussian distribution of BP values obtained over a period of time conceals this. The search for more statistically valid analyses needs to be pursued. Northwick Park Hospital and Clinical Research Centre, Harrow, Middlesex HA1 3UJ
STEWART MANN MICHAEL MILLAR-CRAIG E. B. RAFTERY
SELECTIVE EPIDURAL ANALGESIA
SIR,-We agree with Dr Scott and Dr McClure (June 30, that the administration of opiates via the epidural is a useful method of providing postoperative analgesia. For several months now we have been assessing epidural fentanyl (supplied without preservative) as an alternative form of analgesia after elective caesarean section. All the patients studied so far have had their operations done under epidural analgesia by a conventional local analgesic technique combining lignocaine and bupivacaine. The epidural catheter has been left in situ and the patients asked to request further analgesia when required. This has been provided with 0.11 mg fentanyl diluted with 8 ml 0.9% sodium chloride administered with the patient supine.
p.
1410)
route
1.
Millar-Craig MW, Kenny D, Mann S, Balasubramanian V, Raftery, EB.
Br
Med J 1979; i: 237. 2. Raftery EB, Millar-Craig MW, Mann S, Balasubramanian V. Br Med J 1979; i: 687. 3. Millar-Craig MW, Mann S, Balasubramanian V, Raftery EB. Clin Sci Molec Med 1978; 55: 391-3s. 4. Mann S, Millar-Craig MW, Altman D, Melville DI, Raftery EB. Clin Sci (in
press). 5. Mann S, Millar-Craig MW, Balasubramanian V, Melville DI, Raftery EB. In: Viskaldix in the treatment of hypertension. Medical Education Service Ltd (in press). 6. Raftery EB, Millar-Craig MW. In: Clement D, ed. Blood pressure variability. Lancaster: M.T.P. Press, 1979: 53-65. 7. Mann S, Millar-Craig MW, Melville DI, Balasubramanian V, Raftery EB Clin Sci (in press). 8. Sayers BMcA, Ellis NW, Green HL. Minimum and maximum requirements for physiological measurement: intra-arterial blood pressure: a pilot study report. Engineering in Medicine Laboratory, Imperial College, London, 1978.
acid) were normal, as were chest, abdominal, and skull X-rays. At this stage the patient and her family refused to cooperate and demanded surgical treatment of a presumed insulinoma. A distal pancreatectomy was done, but the pancreas delic
macroscopically and histologically normal. The patient made a good postoperative recovery and her blood-glucose was
remained normal. At this time the results of insulin assays
Barnet General Herts
off
on
A. STELLON N. H. TOWNELL*
Hospital,
*Present address: Academic don NW3 2QG.
Department
of Surgery,
Royal
Free
Regional Respiratory Laboratory,
ster-
T.H. LEE W.M. SEYMOUR
Brook General Hospital, London SE18 4LW
on
admission became available. They were samples In view of this serum-C-peptide levels (see table). very high were measured and found to be suppressed. A search uf the patient’s house then revealed a hidden store of syringes and needles. This case reinforces Scarlett’s opinion that C-peptide levels be measured as an initial investigation in all patients with hypogtycxmia and hyperinsulinism. In our case major surgery would thus have been avoided. sent
ing is symptomatic, and, although our patient was given oids, there is no good evidence to support their efficacy.44
Hospital, Lon-
CAPTOPRIL EFFECT ON HYPERTENSION IN PATIENT WITH RENIN-PRODUCING TUMOUR
SiR,-Primary reninism is a rare syndrome caused by juxtaglomerular cell tumours of the kidneys some Wilms’ tumours,7 and occasionally by other renin-producing neoplasmaWe have seen a case of malignant renin-producing tumour with the full-blown picture or primary reninism, including severe hypertension and secondary aldosteronism. This patient was treated with the angiotensin-i-converting-enzyme inhibitor, captopril (SQ 14225).9 The patient is a 32-year-old woman with one healthy child. She was in perfect health until September, 1975, when hypertension was discovered. Because of poor blood-pressure control with hydrochlorothiazide and propranolol, the patient was
PNEUMONITIS CAUSED BY PETROL SIPHONING
SIR,-Robinson’ has described one hazard of petrol shortages-perioral erythema from siphoning petrol into the mouth. As prices rise and petrol becomes scarce, medical problems due to petrol siphoning may become more common. We have seen a patient with pneumonitis caused in this way. A previously healthy 22-year-old man was siphoning petrol when he sucked about half a cupful into his mouth. He had severe pain in his throat and lost consciousness for a few minutes. He was asymptomatic after this, but thought he had better be seen in the casualty department because of his loss of consciousness. When he was seen, there was a strong smell of petrol but there were no other abnormal signs. However, a chest X-ray showed right-middle-lobe shadowing. His arterial blood gases deteriorated over 4 h from pH 7.32, P02 11 kPa (lkPa=7.5 mm Hg), PC02 4-2 kPa, bicarbonate 15.5 mmol/1, to pH 7.36, POz 5.2 kPa, PC02 4.4 kPa, bicarbonate 18.5 5 mmol/l, despite 1 g methylprednisolone. Over the next 2 days, he needed 40% oxygen to keep his arterial oxygen within the normal range. During this time he coughed up a few specks of blood on one occasion but was otherwise symptom-free and his peak expiratory flow-rate (PEFR) was normal. He was able to maintain a normal PaOz breathing air from the 4th day onwards. However, his chest X-ray showed no change during his week in hospital. Formal respiratory-function tests on the 5th day of his illness were normal and the chest X-ray 1 month later was very much improved. The localised pneumonitis caused by petroleum distillates is thought to be due to aspiration (their low surface tension would facilitate their spread along mucosal surfaces) rather than inhalation of fumes or absorption.23For this reason, many clinicians would be reluctant to subject these patients to gastric lavage or other measures to induce vomiting. However, this man’s pulmonary problems must have been more widespread than the X-ray suggested because his hypoxia seemed incompatible with such a localised abnormality in his middle lobe. The lack of generalised radiological shadowing during his illness would be against an alveolitis, and his normal PEFR would exclude any significant large-airway disease. We suggest that the hypoxia may have been due to a ventilation-perfusion mismatch from bronchiolitis, which resolved over the 4 days, in addition to the more obvious abnormality in the right middle lobe. The treatment for petroleum poison1. Robinson BL. The hazard of petrol shortage. Br Med J 1973; iv: 614. 2. Baldachin BJ, Melmed RN. Clinical and therapeutic aspects of kerosene poisoning:a series of 200 cases. Br Med J 1964; ii: 28-30. 3 Richardson JA, Pratt Thomas HR. Toxic effects of varying doses of kerosene administered by different routes. Am J Med Sci 1951; 221: 531-6.
-1
01
2
3
4
56
Hours
Blood-pressure response to captopril in patient with hypertension due to renin-producing tumour. admitted to hospital in August, 1976. A large pelvic tumour and persistent hypokalaemia were found. After removal of a large tumour (grapefruit sized) adjacent to the normal left ovary, the hypertension and hypokalsemia disappeared. The true nature of the tumour, which was malignant histologically, could not be established. Hypertension and hypokalaemia recurred 9 months later. Investigations suggested primary reninism from recurrent tumour growth. The blood-pressure was 240/130 mm Hg and serum-potassium 3.2 mmol/l. Plasma-renin-activity was 150 ng/ml/h (normal range 03-2.0), plasma-aldosterone 5.0 MI, Chicoine L, Legeve G, Hillman E. Adrenocorticosteroid treatof hydrocarbon pneumonia in children: a cooperative study.J Pediat 1972; 81: 366-9. 5. Robertson PW, Klidjian A, Harding LK, Walters G, Lee MR, Robb-Smith 4. Marks
ment
AHT.
Hypertension
due
to a
renin-secreting
renal
tumor.
Am
J
1967; 43: 963-76. 6. Kihara J, Kitamura S, Hoshimo T, Seida H, Watanabe T. A hitherto
Med
unre-
ported vascular tumour of the kidney: a proposal of "juxtaglomerular cell tumour". Acta Path Jap 1968; 18: 197-206. 7. Mitchell JD, Baxter TJ, Blair-West JR, McCardie DH. Renin levels in nephroblastoma (Wilms’ tumour): report of a renin-secreting tumour. Arch Dis Child 1970; 45: 376-84. 8. Genest J, Rojo Ortega JM, Kuchel O, Boucher R, Nowaczynski W, Lefebvre R, Chretien M, Cantin J, Granger P. Malignant hypertension with hypokalemia in a patient with renin-producing pulmonary carcinoma. Trans Assoc Am Phys 1975; 88: 192-201. 9. Ondetti MA, Rubin B, Cushman DW. Design of specific inhibitors of angiotensin-converting enzyme: new class of orally active antihypertensive agents. Science 1977; 196: 441-4.
150
nmo1/l (0-3-0-8), and urinary aldosterone 300 nmol/day (<56). At angiography the kidneys and the renal arteries were normal. Catheterisation of the cava vena inferior revealed high renin values at all levels. At operation (May, 1978) a large amount of tumour was removed from peritoneum and omentum, as was a big tumour close to the liver. Tumour tissue contained 1-6 Goldblatt units of renin per gram tissue (with reference to the M.R.C. standard). Kidneys from non-renovascular, hypertensive patients contain less than 0.05 units/g, but kidneys from renovascular patients may reach 1 unit/g. After surgery blood-pressure and plasma-renin fell to normal. The patient remained in good condition for about 6 months, when hypertension returned and renin values rose. This time plasma-renin-activity was 80-132 ng/ml/h, and she was readmitted February, 1979. The patient was put on captopril and her blood-pressure responded to 25 and 50 mg (see figure). The blood-pressure fall was dramatic, and on 150 mg three times a day by mouth the patient remained normotensive. Signs of aldosteronism subsided within a week. A new investigation revealed tumour growth close to the liver and at operation in April, 1979, tumour growth was observed in other parts of the abdomen. All visible tumour was removed, but the patient remained hypertensive after this operation. Treatment with captopril 50 mg three times a day has kept blood-pressure normal since then. To our knowledge, this is the first report of the efficacy of captopril in a patient with a renin-producing tumour. The drug was very effective in maintaining normal blood-pressure and serum-potassium without any secondary effects. Departments of Nephrology, Endocrinology, Surgery and Pathology, Sahlgrenska Sjukhuset, S413 45 Göteborg, Sweden, and Department of Medicine, Centrallasarettet, Mölndal
M. AURELL
A. RUDIN L.-E. TISELL L. G. KINDBLOM G. SANDBERG
LOWERING BLOOD-PRESSURE
SIR,-Dr Stewart (April 21, p. 861) claims to have demonstrated that "the relative risk of myocardial infarction in patients with FDP [final diastolic pressure] reduced to <90 mm Hg was more than five times that in patients with FDP 100-109 mm Hg (p<0.01)". He does not state how his statistical analyses were carried out, but the flaw in this study is readily apparent in fig. 1, which shows the frequency distribution of FDPs in 169 patients, 29 of whom had a myocardial infarction and 140 of whom did not. Whatever analysis Stewart used relied heavily on a unimodal distribution of non-myocardial infarction and a bimodal distribution of myocardial infarction. If we take at face value the fact that the myocardial infarction group is truly a bimodal population, then it naturally follows that the incidence of myocardial infarction at the left-hand side of the frequency pressure histogram will be greater in these low-pressure patients. This leads to a statistical problem of comparing bimodal with unimodal populations, a problem which Stewart does not discuss. Moreover, the bimodality of the very small myocardial infarction group is dependent upon the presence of only 3 patients in the 80-85 mm Hg myocardial infarction group. Statisticians would not consider bimodality proved in this group of only 29 patients, and the conclusion that there is an increased incidence of myocardial infarction in the low-pressure group cannot be valid statisti-
cally. Although Stewart claims to have controlled all the risk factors for myocardial infarction in each group, 3 of his 29 myocardial infarction group had hypercholesterolsemia, while only 2 out of 140 non-infarct patients had this feature. Stewart’s conclusions remain only a hypothesis. V. A.
Hospital,
Tucson, Arizona 85723, U.S.A., and Renal Section,
University of Arizona College of Medicine
MURRAY A. KATZ
ONCE-DAILY &bgr;-ADRENOCEPTOR ANTAGONISTS AND ARTERIAL PRESSURE
SIR,-It was with great interest that we read the paper on the influence of once-daily administration of p-adrenoceptor antagonists on arterial pressure and its variability by Dr Watson and colleagues (June 9, p. 1210). That many, if not all, of the available beta blockers have a hypotensive action lasting well beyond 24 h from the time of last administration is substantiated by many non-invasive studies and also by our own study on atenoloP which Watson et al. cite. However, a lack of consistency in the effect on night-time and early-morning blood-pressure (BP) should not be confused with duration of action of the drugs, the former being ascertainable almost exclusively by this form of ambulatory monitoring. We do not feel that the lack of an early-morning effect is a universal feature of beta blockers,2 even when given once daily, since other studies from our unit have shown variable responses.3-5 It is a pity that Watson et al. did not feel able to separate their results according to drug taken. One apparently consistent observation is that groups of patients with higher pretreatment BP (and by inference, necessarily poorer control with monotherapy) show the greatest tendency towards lack of early-morning BP control. The pretreatment data of Watson et al. show a post-waking rise in BP before the patient rises from bed, confirming our results. 6,7 We agree that BP variability is probably important in the mechanism of cardiovascular disease. The validity of using standard deviation (or variance) of a given period of recorded signal in this way is however questionable given the nonstationarity of the dataeven with the partial control of physical activity during their studies. The apparent gaussian distribution of BP values obtained over a period of time conceals this. The search for more statistically valid analyses needs to be pursued. Northwick Park Hospital and Clinical Research Centre, Harrow, Middlesex HA1 3UJ
STEWART MANN MICHAEL MILLAR-CRAIG E. B. RAFTERY
SELECTIVE EPIDURAL ANALGESIA
SIR,-We agree with Dr Scott and Dr McClure (June 30, that the administration of opiates via the epidural is a useful method of providing postoperative analgesia. For several months now we have been assessing epidural fentanyl (supplied without preservative) as an alternative form of analgesia after elective caesarean section. All the patients studied so far have had their operations done under epidural analgesia by a conventional local analgesic technique combining lignocaine and bupivacaine. The epidural catheter has been left in situ and the patients asked to request further analgesia when required. This has been provided with 0.11 mg fentanyl diluted with 8 ml 0.9% sodium chloride administered with the patient supine.
p.
1410)
route
1.
Millar-Craig MW, Kenny D, Mann S, Balasubramanian V, Raftery, EB.
Br
Med J 1979; i: 237. 2. Raftery EB, Millar-Craig MW, Mann S, Balasubramanian V. Br Med J 1979; i: 687. 3. Millar-Craig MW, Mann S, Balasubramanian V, Raftery EB. Clin Sci Molec Med 1978; 55: 391-3s. 4. Mann S, Millar-Craig MW, Altman D, Melville DI, Raftery EB. Clin Sci (in
press). 5. Mann S, Millar-Craig MW, Balasubramanian V, Melville DI, Raftery EB. In: Viskaldix in the treatment of hypertension. Medical Education Service Ltd (in press). 6. Raftery EB, Millar-Craig MW. In: Clement D, ed. Blood pressure variability. Lancaster: M.T.P. Press, 1979: 53-65. 7. Mann S, Millar-Craig MW, Melville DI, Balasubramanian V, Raftery EB Clin Sci (in press). 8. Sayers BMcA, Ellis NW, Green HL. Minimum and maximum requirements for physiological measurement: intra-arterial blood pressure: a pilot study report. Engineering in Medicine Laboratory, Imperial College, London, 1978.