673
Conservative management of peptic ulcer
perforated
SIR,—In your Dec 16 editorial you discuss the conservative management of perforated peptic ulcer. The idea of treating such patients non-operatively remains anathema to many general surgeons. 2 years ago we adopted a conservative policy for treating those patients with perforated peptic ulcer who fulfilled strict criteria. The diagnosis was made both on clinical grounds and on the finding of gas under the diaphragm on an erect chest radiograph. The criteria used for treating patients non-operatively are duration of acute symptoms less than 24 h, radiological placement of a nasogastric tube in the antrum of the stomach and continuous aspiration, intravenous fluids, and an H2-antagonist. Patients not fulfilling these criteria or clinically not improving have surgical treatment.
Since the inception of this policy, thirty patients with perforated peptic ulcer have presented to the five surgeons in this hospital. Ten male and eight female patients (median age 58 years, range 29-77)
Fig 1-Scheme of endoscope and scaled tube. LOD=a+b.
a
suitable for conservative management. None have died; two needed operative intervention because of worsening clinical signs at 12 and 36 hours; two had subphrenic collections which were successfully drained percutaneously; and one reperforated at 3 months. Three patients were aged over 70 years; one needed operative intervention and another had percutaneous drainage of a subphrenic collection. The median duration of hospital stay was 9 days (range 5-24), whereas for those with non-complicated conservative management it was 7 days (range 5-11). Six male and eight female patients (median age 71, range 27-77) were not suitable for (12 patients) or did not improve with (two patients) conservative management and had surgical treatment (simple oversew in twelve, vagotomy and pyloroplasty in one, partial gastrectomy in one), with no deaths. One patient had a subphrenic collection which was drained operatively, one subsequently had pyloric stenosis, and another had small bowel obstruction. The median duration of hospital stay was 11 days were
is fixed, 6 is variable and determines LOD.
(range 5-23). Fig 2-Photograph of lesion viewed endoscopically and of 2 mm graph paper. Polyp shown measures 7 mm in diameter tube 2 or 3 cm from the tip is used to measure the distance between the lesion and the tip of the endoscope (LOD). The tube is extruded from the endoscope channel until its tip touches the lesion; a photograph of the lesion and the graduations on the tube is taken. LOD is measured by the graduations in the photograph (fig 1). The area and the length of lesions is then measured by comparison of a photograph of the lesion with that of graph paper taken at the same
LOD (fig 2). We used two bronchofibrescopes and a gastrofibrescope (BF type
4B2, BF type IT10, GIF type P3, Olympus, Tokyo)
to measure
several
objects to confirm the precision of this method. For example, we measured a circle 4 mm in diameter 10 times, and the maximum error was less than 0-5 mm (mean 3-98 mm, SD 0-24). Gastroendoscopic measurements were compared with radiographic techniques or samples obtained at operations. The results were similar to those of the samples and were not enlarged, as they were on radiographs. This method is easy to do, safe, and can be widely used since it does not require special instruments. Department of Medicine, Kurume University School of Medicine, Kurume, Fukuoka, Japan 1.
T. RIKIMARU Y. ICHIKAWA
M. KAJI
Sonnenberg A, Giger M, et al. How reliable is determination of ulcer size by endoscopy? Br Med J, 1979; 24: 1322-24. 2 Dancygier H, Wurbs D, Classen M. A new method for the endoscopic determination of gastrointestinal ulcer area. Endoscopy 1981; 13: 214-16. 3 Ohida M, Okada N, et al. Basic studies on marker disk method for endoscopic determination of gastric ulcer area. Gastroenterol Endosc 1982; 24: 225-33. 4. Monaco AP, Roth SI, Castleman B, Welch CE. Adenomatous polyps of the stomach. Cancer 1962; 15: 456-67.
With the provision that strict criteria are adhered to, nonoperative management of perforated peptic ulcer carries no excess mortality or morbidity in our or others’ hands.l,2 The duration of hospital stay is also decreased. The worry of wrong diagnosis is reduced to a minimum since the treatment instituted is standard resuscitation. If the patient fails to respond surgery can be done immediately. We agree that close clinical observation and the involvement of a senior surgeon is mandatory, especially in patients over 70 years old. The implications of the confidential inquiry into perioperative deaths and the blossoming of clinical audit reveals that surgical management of perforated peptic ulcer is not the only option in the surgeon’s armamentarium. KEITH M. RIGG ROBERT C. STUART Stockton on Tees. Cleveland TS19 8PE, UK I. LAURENCE ROSENBERG 1. Taylor H. The non-surgical treatment of perforated peptic ulcer. Gastroenterology Department of Surgery, North Tees General Hospital,
1957; 33: 353-68. TE, Dillon B, Afdal NH, McCormack CJ. Conservative management of perforated duodenal ulcer. Br J Surg 1988; 75: 583-84.
2. Keane
Drug compliance in asthma SIR,-Your Feb 3 editorial prompts me to expand on the observation that "factors leading to poor compliance need to be determined". In our acute asthma unit (where over 2500 cases are admitted yearly), I have developed an approach to non-compliance that may be useful to Lancet readers. Non-compliance may be viewed as a symptom-like headache. The inexperienced clinician’s reflex is to surrender responsibility at first sight of this symptom, whereas he/she should recognise therein the need for a constructive therapeutic alliance. A closer definition of the "non-compliance syndrome" invariably suggests strategies for intervention that are (usually) effective. Six syndromes of non-compliance in asthmatics may be discerned. (1) Patient ignorance. For example, the patient has never been told why prophylaxis with steroids (inhalers or systemic) will bring
674 about long-term stability, noticeable. The solution is
even though immediate benefit is not patient education. (2) Inadequate cognitive abilities. This may not be evident to the clinician unless every consultation includes the question, "Now, please tell me exactly what drugs you took last night and this morning". The solution is to write a daily "user-friendly" schedule or obtain the help of a responsible adult to supervise treatment at
LABORATORY FINDINGS IN CHILD WITH FOCAL SCLEROSING GLOMERULONEPHRITIS BEFORE AND AFTER TREATMENT WITH FK 506
home.
(3) Inadequate personality. Some patients have adequate cognitive functions, but perform poorly under stress. The solution is that for (2). (4) Escape. Some asthmatics stop taking their drugs in order to escape to hospital (eg, a child who is being molested or a mother who is greatly stressed at home). The solution is sensitive diagnostic and therapeutic counselling with the aid of social workers and others. (5) Pseudo non-compliance. For example, failure to recognise that labile asthmatics may have attacks despite rigid adherence to inadequate medical therapy—eg, a subtherapeutic serum theophylline concentration may result from an efficient liver, the patient sometimes needing 3 or 4 times the standard dose of slow-release xanthines. The solution lies in efforts to recognise such asthmatics and rapid metaboliers (the latter by plotting a pharmacokinetic curve in the clinic). (6) "Medical Munchausen’s syndrome".This is the rare lonely patient who enjoys the attention of a medical admission. The solution here is a supportive professional attitude, with the invitation to attend outpatient clinics and educational sessions more often and, for example, exchanging Christmas cards. A logical, systematic approach to such non-compliance, although time-consuming, usually yields the reward of reducing the risk of acute asthma attacks and enhancing the patient’s (and the doctor’s) quality of life. Respiratory Clinic, Groote Schuur Hospital and University of Cape Town, 7925 Observatory, Cape Town, South Africa
S.
J. LOUW
FK 506 in steroid-resistant focal sclerosing glomerulonephritis of childhood
Conversion factors creatinine mmol/I = mg/dl x 88 4, BUN cholesterol mmol/I mg/dl- — 38 7, albumin g/i =g/dl x 10. *FK 506 started Nov 20,1989
successful treatment of cyclosporin-induced haemolytic uraemic syndrome suggests that FK 506 may be effective in many renal and extrarenal immunomediated disorders. Cautious attempts are appropriate to reduce the FK 506 dose. There is no reason to assume that the present dose will be needed for maintenance. The immediate response ofa 41-year-old man has been similar to that of this child. He had mesangial proliferative glomerulonephritis and steroid-resistant nephrosis for 6 months (6-10 g daily urinary protein) before he was treated with 0- 15 mg/kg FK 506 starting on Feb 13, 1990, and with the discontinuance of prednisone 100 mg daily. Within the next 10 days, urinary protein declined to 1485 mg, serum cholesterol fell from 360 to 240 mg/dl, and creatinine clearance remained the same. as our
Supported by research grants from the Veterans Administration and project grant no DK 29961 from the National Institutes of Health.
SIR,-Focal sclerosing glomerulonephritis (FSGN) is the leading of steroid-resistant nephrotic syndrome in childhood. Cytotoxic agents may induce remission but jeopardise future fertility. Cyclosporin has reduced proteinuria at the cost of progressive renal failure, to which drug nephrotoxicity probably contributes.1,2 We have used FK 506 to treat FSGN. Periorbital and peripheral oedema developed in a previously healthy 19-month-old boy in November, 1988. Urinalysis revealed 4+ protein but was otherwise unremarkable. Creatinine was 0-7 mg/dl, blood urea/nitrogen (BUN) 16 mg/dl, albumin 1.8 g/dl and serum cholesterol 411 mg/dl (for conversion factors see table). Antinuclear antibodies, C3, C4, hepatitis B screen, and antistreptolysin-0 titres were normal. Prednisone (175 mg daily) was started but proteinuria was not reduced during 7 months of treatment and steroids were tapered to 35 mg daily. Increasing peripheral oedema and ascites led to two hospital admissions for intravenous diuretic therapy. Renal biopsy after 9 months showed focal and segmental glomerulosclerosis with moderate interstitial fibrosis. A course of cyclophosphamide did not alter the proteinuria. At 30 months of age he was referred to us with grossly cushingoid features and anasarca. He was receiving high-dose loop diuretics and metolazone. Oral FK 506 (0-15 mg/kg twice daily) was started and prednisone was reduced to 5 mg daily, and after 4 weeks was stopped. There was dramatic and progressive improvement clinically and in the laboratory findings (table). Diuretics were discontinued. He has had no side-effects of FK 506 after 15 of weeks of treatment. Complete remission of FSGN occurred in this child without a reduction in renal function, something not recorded previously in cyclosporin-induced remission of FSGN and other forms of steroid-resistant nephrotic syndrome.!-4 We have reported that FK 506 in liver transplant recipients is more potent and less nephrotoxic than cyclosporin.Our observations in this child as well cause
mmol/I = mg/dl-6,
"=
JERRY MCCAULEY Departments of Medicine and Surgery, University Health Center of Pittsburgh, University of Pittsburgh, and Veterans Administration Medical Center,
Pittsburgh PA 15213, USA
ANDREAS G. TZAKIS JOHN J. FUNG SATORU TODO THOMAS E. STARZL
JM, Andreas A, Prieto C, Praga M, Gutierrez VM, Rodicio JL Cyclosporin-induced partial and transient improvement of nephrotic syndrome m recurrent focal segmental glomerulosclerosis. Nephron 1989; 53: 283-84. 2. James RW, Burke JR, Petrie JJ, Rigby RJ, Williams M. Cyclosporin A in the treatment of childhood glomerulonephritis. Aust NZ J Med 1989; 19: 198-201. 3. Lagrue G, Laurent J, Robeva R. Membranoproliferative glomerulonephritis associated with Buckley’s syndrome, treated with cyclosporin. Nephron 1986; 44: 1. Morales
382-83.
Tumey JH, Adu D, Michael J, McMaster P. Recurrent crescentic glomerulonephritis in renal transplant recipient treated with cyclosporin. Lancet 1986; i: 1104 5. McCauley J, Fung J, Jain A, Todo S, Starzl TE. The effects of FK 506 on renal function after liver transplantation. Transplant Proc 1990; 22 (suppl 1): 13-16. 6. McCauley J, Bronsther O, Fung J, Todo S, Starzl TE. Treatment of cyclospornninduced haemolytic uraemic syndrome with FK 506. Lancet 1989; ii: 1516.
4.
CORRECTIONS Drug economics In developing countnes In this letter by Dr J. I. Litvack colleagues (Jan 6, p 61) the last sentence should have read "Our analysis experience from several countries suggest that substantial cost recovery
and and can
be achieved ...".
Effect of diarrhoeal disease control on infant and childhood mortahty In Egypt In the results section of this article by Dr El-Rafie and colleagues (Feb 10, p 334) the number of MOH and university clinics and hospitals should have been 3200 and not 32 000.
Conservative management of peptic ulcer
perforated
SIR,—In your Dec 16 editorial you discuss the conservative management of perforated peptic ulcer. The idea of treating such patients non-operatively remains anathema to many general surgeons. 2 years ago we adopted a conservative policy for treating those patients with perforated peptic ulcer who fulfilled strict criteria. The diagnosis was made both on clinical grounds and on the finding of gas under the diaphragm on an erect chest radiograph. The criteria used for treating patients non-operatively are duration of acute symptoms less than 24 h, radiological placement of a nasogastric tube in the antrum of the stomach and continuous aspiration, intravenous fluids, and an H2-antagonist. Patients not fulfilling these criteria or clinically not improving have surgical treatment.
Since the inception of this policy, thirty patients with perforated peptic ulcer have presented to the five surgeons in this hospital. Ten male and eight female patients (median age 58 years, range 29-77)
Fig 1-Scheme of endoscope and scaled tube. LOD=a+b.
a
suitable for conservative management. None have died; two needed operative intervention because of worsening clinical signs at 12 and 36 hours; two had subphrenic collections which were successfully drained percutaneously; and one reperforated at 3 months. Three patients were aged over 70 years; one needed operative intervention and another had percutaneous drainage of a subphrenic collection. The median duration of hospital stay was 9 days (range 5-24), whereas for those with non-complicated conservative management it was 7 days (range 5-11). Six male and eight female patients (median age 71, range 27-77) were not suitable for (12 patients) or did not improve with (two patients) conservative management and had surgical treatment (simple oversew in twelve, vagotomy and pyloroplasty in one, partial gastrectomy in one), with no deaths. One patient had a subphrenic collection which was drained operatively, one subsequently had pyloric stenosis, and another had small bowel obstruction. The median duration of hospital stay was 11 days were
is fixed, 6 is variable and determines LOD.
(range 5-23). Fig 2-Photograph of lesion viewed endoscopically and of 2 mm graph paper. Polyp shown measures 7 mm in diameter tube 2 or 3 cm from the tip is used to measure the distance between the lesion and the tip of the endoscope (LOD). The tube is extruded from the endoscope channel until its tip touches the lesion; a photograph of the lesion and the graduations on the tube is taken. LOD is measured by the graduations in the photograph (fig 1). The area and the length of lesions is then measured by comparison of a photograph of the lesion with that of graph paper taken at the same
LOD (fig 2). We used two bronchofibrescopes and a gastrofibrescope (BF type
4B2, BF type IT10, GIF type P3, Olympus, Tokyo)
to measure
several
objects to confirm the precision of this method. For example, we measured a circle 4 mm in diameter 10 times, and the maximum error was less than 0-5 mm (mean 3-98 mm, SD 0-24). Gastroendoscopic measurements were compared with radiographic techniques or samples obtained at operations. The results were similar to those of the samples and were not enlarged, as they were on radiographs. This method is easy to do, safe, and can be widely used since it does not require special instruments. Department of Medicine, Kurume University School of Medicine, Kurume, Fukuoka, Japan 1.
T. RIKIMARU Y. ICHIKAWA
M. KAJI
Sonnenberg A, Giger M, et al. How reliable is determination of ulcer size by endoscopy? Br Med J, 1979; 24: 1322-24. 2 Dancygier H, Wurbs D, Classen M. A new method for the endoscopic determination of gastrointestinal ulcer area. Endoscopy 1981; 13: 214-16. 3 Ohida M, Okada N, et al. Basic studies on marker disk method for endoscopic determination of gastric ulcer area. Gastroenterol Endosc 1982; 24: 225-33. 4. Monaco AP, Roth SI, Castleman B, Welch CE. Adenomatous polyps of the stomach. Cancer 1962; 15: 456-67.
With the provision that strict criteria are adhered to, nonoperative management of perforated peptic ulcer carries no excess mortality or morbidity in our or others’ hands.l,2 The duration of hospital stay is also decreased. The worry of wrong diagnosis is reduced to a minimum since the treatment instituted is standard resuscitation. If the patient fails to respond surgery can be done immediately. We agree that close clinical observation and the involvement of a senior surgeon is mandatory, especially in patients over 70 years old. The implications of the confidential inquiry into perioperative deaths and the blossoming of clinical audit reveals that surgical management of perforated peptic ulcer is not the only option in the surgeon’s armamentarium. KEITH M. RIGG ROBERT C. STUART Stockton on Tees. Cleveland TS19 8PE, UK I. LAURENCE ROSENBERG 1. Taylor H. The non-surgical treatment of perforated peptic ulcer. Gastroenterology Department of Surgery, North Tees General Hospital,
1957; 33: 353-68. TE, Dillon B, Afdal NH, McCormack CJ. Conservative management of perforated duodenal ulcer. Br J Surg 1988; 75: 583-84.
2. Keane
Drug compliance in asthma SIR,-Your Feb 3 editorial prompts me to expand on the observation that "factors leading to poor compliance need to be determined". In our acute asthma unit (where over 2500 cases are admitted yearly), I have developed an approach to non-compliance that may be useful to Lancet readers. Non-compliance may be viewed as a symptom-like headache. The inexperienced clinician’s reflex is to surrender responsibility at first sight of this symptom, whereas he/she should recognise therein the need for a constructive therapeutic alliance. A closer definition of the "non-compliance syndrome" invariably suggests strategies for intervention that are (usually) effective. Six syndromes of non-compliance in asthmatics may be discerned. (1) Patient ignorance. For example, the patient has never been told why prophylaxis with steroids (inhalers or systemic) will bring
674 about long-term stability, noticeable. The solution is
even though immediate benefit is not patient education. (2) Inadequate cognitive abilities. This may not be evident to the clinician unless every consultation includes the question, "Now, please tell me exactly what drugs you took last night and this morning". The solution is to write a daily "user-friendly" schedule or obtain the help of a responsible adult to supervise treatment at
LABORATORY FINDINGS IN CHILD WITH FOCAL SCLEROSING GLOMERULONEPHRITIS BEFORE AND AFTER TREATMENT WITH FK 506
home.
(3) Inadequate personality. Some patients have adequate cognitive functions, but perform poorly under stress. The solution is that for (2). (4) Escape. Some asthmatics stop taking their drugs in order to escape to hospital (eg, a child who is being molested or a mother who is greatly stressed at home). The solution is sensitive diagnostic and therapeutic counselling with the aid of social workers and others. (5) Pseudo non-compliance. For example, failure to recognise that labile asthmatics may have attacks despite rigid adherence to inadequate medical therapy—eg, a subtherapeutic serum theophylline concentration may result from an efficient liver, the patient sometimes needing 3 or 4 times the standard dose of slow-release xanthines. The solution lies in efforts to recognise such asthmatics and rapid metaboliers (the latter by plotting a pharmacokinetic curve in the clinic). (6) "Medical Munchausen’s syndrome".This is the rare lonely patient who enjoys the attention of a medical admission. The solution here is a supportive professional attitude, with the invitation to attend outpatient clinics and educational sessions more often and, for example, exchanging Christmas cards. A logical, systematic approach to such non-compliance, although time-consuming, usually yields the reward of reducing the risk of acute asthma attacks and enhancing the patient’s (and the doctor’s) quality of life. Respiratory Clinic, Groote Schuur Hospital and University of Cape Town, 7925 Observatory, Cape Town, South Africa
S.
J. LOUW
FK 506 in steroid-resistant focal sclerosing glomerulonephritis of childhood
Conversion factors creatinine mmol/I = mg/dl x 88 4, BUN cholesterol mmol/I mg/dl- — 38 7, albumin g/i =g/dl x 10. *FK 506 started Nov 20,1989
successful treatment of cyclosporin-induced haemolytic uraemic syndrome suggests that FK 506 may be effective in many renal and extrarenal immunomediated disorders. Cautious attempts are appropriate to reduce the FK 506 dose. There is no reason to assume that the present dose will be needed for maintenance. The immediate response ofa 41-year-old man has been similar to that of this child. He had mesangial proliferative glomerulonephritis and steroid-resistant nephrosis for 6 months (6-10 g daily urinary protein) before he was treated with 0- 15 mg/kg FK 506 starting on Feb 13, 1990, and with the discontinuance of prednisone 100 mg daily. Within the next 10 days, urinary protein declined to 1485 mg, serum cholesterol fell from 360 to 240 mg/dl, and creatinine clearance remained the same. as our
Supported by research grants from the Veterans Administration and project grant no DK 29961 from the National Institutes of Health.
SIR,-Focal sclerosing glomerulonephritis (FSGN) is the leading of steroid-resistant nephrotic syndrome in childhood. Cytotoxic agents may induce remission but jeopardise future fertility. Cyclosporin has reduced proteinuria at the cost of progressive renal failure, to which drug nephrotoxicity probably contributes.1,2 We have used FK 506 to treat FSGN. Periorbital and peripheral oedema developed in a previously healthy 19-month-old boy in November, 1988. Urinalysis revealed 4+ protein but was otherwise unremarkable. Creatinine was 0-7 mg/dl, blood urea/nitrogen (BUN) 16 mg/dl, albumin 1.8 g/dl and serum cholesterol 411 mg/dl (for conversion factors see table). Antinuclear antibodies, C3, C4, hepatitis B screen, and antistreptolysin-0 titres were normal. Prednisone (175 mg daily) was started but proteinuria was not reduced during 7 months of treatment and steroids were tapered to 35 mg daily. Increasing peripheral oedema and ascites led to two hospital admissions for intravenous diuretic therapy. Renal biopsy after 9 months showed focal and segmental glomerulosclerosis with moderate interstitial fibrosis. A course of cyclophosphamide did not alter the proteinuria. At 30 months of age he was referred to us with grossly cushingoid features and anasarca. He was receiving high-dose loop diuretics and metolazone. Oral FK 506 (0-15 mg/kg twice daily) was started and prednisone was reduced to 5 mg daily, and after 4 weeks was stopped. There was dramatic and progressive improvement clinically and in the laboratory findings (table). Diuretics were discontinued. He has had no side-effects of FK 506 after 15 of weeks of treatment. Complete remission of FSGN occurred in this child without a reduction in renal function, something not recorded previously in cyclosporin-induced remission of FSGN and other forms of steroid-resistant nephrotic syndrome.!-4 We have reported that FK 506 in liver transplant recipients is more potent and less nephrotoxic than cyclosporin.Our observations in this child as well cause
mmol/I = mg/dl-6,
"=
JERRY MCCAULEY Departments of Medicine and Surgery, University Health Center of Pittsburgh, University of Pittsburgh, and Veterans Administration Medical Center,
Pittsburgh PA 15213, USA
ANDREAS G. TZAKIS JOHN J. FUNG SATORU TODO THOMAS E. STARZL
JM, Andreas A, Prieto C, Praga M, Gutierrez VM, Rodicio JL Cyclosporin-induced partial and transient improvement of nephrotic syndrome m recurrent focal segmental glomerulosclerosis. Nephron 1989; 53: 283-84. 2. James RW, Burke JR, Petrie JJ, Rigby RJ, Williams M. Cyclosporin A in the treatment of childhood glomerulonephritis. Aust NZ J Med 1989; 19: 198-201. 3. Lagrue G, Laurent J, Robeva R. Membranoproliferative glomerulonephritis associated with Buckley’s syndrome, treated with cyclosporin. Nephron 1986; 44: 1. Morales
382-83.
Tumey JH, Adu D, Michael J, McMaster P. Recurrent crescentic glomerulonephritis in renal transplant recipient treated with cyclosporin. Lancet 1986; i: 1104 5. McCauley J, Fung J, Jain A, Todo S, Starzl TE. The effects of FK 506 on renal function after liver transplantation. Transplant Proc 1990; 22 (suppl 1): 13-16. 6. McCauley J, Bronsther O, Fung J, Todo S, Starzl TE. Treatment of cyclospornninduced haemolytic uraemic syndrome with FK 506. Lancet 1989; ii: 1516.
4.
CORRECTIONS Drug economics In developing countnes In this letter by Dr J. I. Litvack colleagues (Jan 6, p 61) the last sentence should have read "Our analysis experience from several countries suggest that substantial cost recovery
and and can
be achieved ...".
Effect of diarrhoeal disease control on infant and childhood mortahty In Egypt In the results section of this article by Dr El-Rafie and colleagues (Feb 10, p 334) the number of MOH and university clinics and hospitals should have been 3200 and not 32 000.
