Outpatient care for selected patients with acute upper gastrointestinal bleeding

lower left percentral gyrus. There were also multiple plaques in a periventricular distribution that did not enhance with gadolinium. 1000 mg prednisolone per day was given for 5 days. Seizures disappeared within the first day of therapy and did not recur even after withdrawal of phenytoin. We have seen two patients with epilepsia partialis continua (one motor, one dysphasic) as the most prominent symptoms of a relapse or presentation of MS. Both patients have definite MS according to the diagnostic criteria of Poser and colleagues.5 MRI .studies showed plaques in localisations where they could be responsible for the clinical symptoms. In both patients symptoms disappeared after initiation of anti-inflammatory therapy and the course was

benign. We suggest that after exclusion of more common causes a relapse of MS should be considered in cases of epilepsia partialis continua in adults. MRI can help in the differentiation from brainstem fits. Anticonvulsants seem to be of limited value under these circumstances and long-term anticonvulsive medication may be not generally indicated because of the relapsing nature of the disease. *Josef Spatt, Georg Goldenberg, Bruno Mamoli Ludwig Boltzmann Institut für Epilepsie, Neurologisches Krankenhaus Rosenhugel, 1130 Vienna, Austria

Number of shown.

1 Ghezzi A, Montanini R, Basso PF, et al. Epilepsy in multiple sclerosis. Eur Neurol 1990; 30: 218-23. 2 Thompson AJ, Kermode AG, Moseley IF, et al. Seizures due to multiple sclerosis: seven patients with MRI correlations. J Neurol Neurosurg Psychiatry 1993; 56: 1317-20. 3 Miller DH, Rudge P, Johnson G, et al. Serial gadolinium enhanced magnetic resonance imaging in multiple sclerosis. Brain 1988; 111: 927-39. 4

5

Spatt J, Goldenberg G, Mamoli B. Simple dysphasic seizures as sole manifestation of a relapse in multiple sclerosis. Epilepsia 1994; 35: 1342-45. Poser CM, Paty DW, Scheinberg L, et al. New diagnostic criteria for multiple sclerosis: guidelines for research proposals. Ann Neurol 1983; 13: 227-31.

Outpatient

care

acute upper

for selected patients with

gastrointestinal bleeding

SiR-Longstreth and Feitelberg (Jan 14, p 108) prospectively assess outpatient care of 34 patients with acute non-variceal upper gastrointestinal haemorrhage. To examine the potential for outpatient care in the UK we have analysed data from the National Audit of Acute Upper Gastrointestinal Haemorrhage, which has obtained data on all patients in hospital with this condition (4185) in four English health regions during 4 months of 1993. 3508 patients with acute upper gastrointestinal bleeding who were acute admissions were identified by the audit, and of these 2740 (78%) were endoscoped and so could provide sufficient for clinical information Longstreth and Feitelberg’s criteria to be applied. Patients who were already in hospital (584) or were transfers from other hospitals (93) were excluded from this analysis. These criteria for outpatient care were interpreted as closely as possible to conform to our database so that patients were excluded from the analysis if they had any one of the following: stigmata of recent haemorrhage; oesophageal or gastric varices; any comorbidity; shock (tachycardia with or without hypotension); haemoglobin less than 80 g/L; anticoagulation therapy or coagulopathy; or presenting symptom or sign of syncope. Because our audit data were not able to identify debilitation or severe liver disease or serious concomitant disease in the same way as in the USA report, any comorbidity recorded was used to cover these terms.

patients (%)

shown. Data for 21 other patients with different

diagnoses

not

Table: Outcome and mean hospital stay in 589 selected patients with acute upper gastrointestinal bleeding

or multiple melaena could not be identified in our data, syncope on presentation was used as a proxy measure in our calculations since we had found it to be independently associated with mortality. Our data could not identify patients with poor social support. With these criteria, of the 2740 patients with acute upper gastrointestinal bleeding having an endoscopy, 589 had none of the criteria listed above on admission (or ascertained soon afterwards) and therefore might have been suitable for outpatient management according to the criteria of Longstreth and Feitelberg. The table shows what happened to these patients according to age and final

Similarly, although large haematemesis

diagnosis. It is clear that diagnoses such as Mallory-Weiss tears, erosions and oesophagitis are associated with few adverse events and might be safely managed as outpatients. If patients with these diagnoses alone were selected for outpatient management, a saving of 1042 bed-days would accrue. This represents 4% of the total bed-days occupied by the 4185 patients identified by the audit. However, 22% of the 589 and 37% of 193 with peptic ulceration were judged to need blood transfusion, which usually means a short admission. Furthermore, when endoscopy revealed either a serious source of bleeding such as ulcer or cancer or no clear source of bleeding, the rebleeding rate approached 8%. The figures for mortality are reassuring; only 1 death was from ulcer bleeding, the other deaths being from bleeding followed by ulcer perforation and following colectomy for bleeding diverticular disease with an ulcer having been detected incidentally at endoscopy. Despite the limitations of a retrospective approach, these data suggest that possibly 20% of patients with upper gastrointestinal bleeding in England could be safely managed as outpatients. The proportion is lower than the USA figure of 30% and possible reasons for differences between the USA and the UK were discussed by Walt in his commentary (p 77). Appropriate selection of patients for outpatient management would require rapid endoscopy and accurate diagnosis. Larger prospective studies with appropriate cost-benefit analyses, are now needed to assess 659

the true value of outpatient management of this medical condition.’1 C J Packham, T A Rockall, *R F A

common

Logan

*Department of Public Health Medicine and Epidemiology, University of Nottingham Medical School, Queen’s Medical Centre, Nottingham NG7 2UH, UK; and Surgical Epidemiology and Audit Unit, Royal College of Surgeons of England, London WC2

Rockall TA, Logan RFA, Devlin HB, Northfield TC. Incidence and mortality of acute upper gastrointestinal bleeding (UGIB) in the UK. Gut 1994; 35 (suppl 5): S47.

1

tissues by in-situ hybridisation, which is generally believed to be less sensitive than RT-PCR. The only fragments we amplified were obtained with nucleocapsid protein gene primers and, by sequencing, they were unrelated to the

nucleocapsid protein

gene,

as

reported.

If the measles virus was really present in such abundance as Wakefield et al’ reported, we believe that any one of four primer pairs that were targeted to diverse regions of the measles virus genome should have picked it up. *Osamu

Nakagomi, Masahiro Iizuka

Departments of *Microbiology and Internal Medicine, Akita University School of Medicine. Akita 010, Japan

Measles virus in Crohn’s disease

1

may be several reasons for Iizuka and failure (Jan 21, p 199) to detect measles virus by colleagues’ reverse transcriptase (RT) PCR in intestinal tissues affected by Crohn’s disease. The first, and most obvious, is that the virus is not there; however, we know that this is not so since we have confirmed the presence of the virus by immunogold electronmicroscopy.’ The alternative explanation is that the experimental approach chosen by Iizuka and co-workers was flawed; they did not include any relevant positive controls, which makes their negative results impossible to interpret. Iizuka and colleagues might have omitted the positive control because it is very difficult to choose an appropriate positive control for their experiment whose aim is to detect a low-copy-number RNA virus that is localised to discrete foci within grossly inflamed tissues. Therefore, without having gone through the essential preliminary steps of determining the optimum conditions and sensitivity of RT-PCR for detection of measles virus in persistently infected human tissues, the application of this technique for the study of Crohn’s disease was ill considered.

2

SiR-There

*A J Wakefield, R E Pounder Department of Medicine, Royal Free Hospital School of Medicine. University of London, London NW3 2PF, UK

1

Lewin J, Dhillon AP, Sim R, et al. Persistent measles virus infection of intestinal tissues: confirmation by immunogold electronmicroscopy. Gut (in press).

<4 users’

reply

SiR-Wakefield and Pounder claim that the absence of controls and a low copy number of measles virus present in the affected tissue of a Crohn’s disease patient (based on their observations’) invalidate our conclusion that measles virus was absent in our Crohn’s disease patient. The RT-PCR protocols we used have been field-tested and validated in laboratories specialising in measles virus (two of the co-authors in our letter have taken part in such research). For example, the high sensitivity of the RT-PCR assay was shown by the findings: for example, the method allowed viral gene amplification from archival serum specimens from 28 years ago of measles patients.2 Samples of the same serum specimens were used as positive controls, although not incorporated in every run of experiments. We did immunohistochemistry (n=10) with the same monoclonal antibody that Wakefield and colleagues’ used to show the nucleocapsid protein of measles virus (Seralab, Crawley Down, UK) and obtained positive staining in all cases, although the positive cells in Crohn’s disease tissues outnumbered those in the controls (Iizuka M, et al, unpublished observation). It is also noteworthy that Wakefield and co-workers’1 detected the measles virus genome (the nucleocapsid protein gene) in Crohn’s disease

positive

660

Wakefield AJ, Pittilo RM, Sim R, et al. Evidence of persistent measles virus infection in Crohn’s disease. J Med Virol 1993; 39: 345-53. Saito H, Nakagomi O, Morita M. Molecular identification of two distinct hemagglutinin types of measles virus by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Mol Cell Probes (in press).

Parvovirus B19 infection during pregnancy treated with high-dose intravenous

gammaglobulin SiR-High-dose intravenous immunoglobulin (IVIG) has to be effective in treating patients with severe B19-parvovirus-induced disorders.’ We report the use of high-dose IVIG to improve maternal and fetal outome in a 34-year-old woman who was admitted at 24 gestational weeks because of signs of severe pre-eclampsia. The fetus had ascites and a huge pericardial effusion compressing the lungs. Cord haemoglobin was 60 g/L. Because of the risk of hypoplasia of the lungs the pericardium was punctured and the effusion aspirated. Maternal blood, fetal blood, and pericardial aspirate were examined for viraP or bacterial infection. While awaiting test results the woman was treated with cefuroxime for possible borrelia infection and corticosteroids for fetal lung maturation. Intermittent injections of diuretics and intravenous albumin were given for severe pre-eclampsia. Parvovirus B19 infection was confirmed by the presence of specific IgM. Parvovirus B 19 DNA was detected by PCR in maternal sera and in aspirate from the fetal pericardium. Maternal serum antinuclear antibody, antineutrophil cytoplasmic antibody, SS-A(Ro), SS-B(La), and rheumatoid factor were all negative, as was fetal serum rheumatoid factor. 1 week after admission the woman was given 25 g immunoglobulin (Gammonativ, Pharmacia) intravenously. After 15 days albuminuria had decreased from 11g per 24 h been shown

to 1-5 g and blood pressure had returned to normal. The fetal ascites and pericardial effusion had disappeared. Cord haemoglobin was 85 g/L. Weekly fetal and maternal surveillance showed normal progress until 32 weeks’ when a caesarean section was done because of placental abruption. Placental histology showed infarctions but no signs of inflammation. The infant weighed 1455 g and had Apgar scores of 8 at 1 min and 10 at 5 min. Haemoglobin was 158 g/L. She was treated in an incubator for 8 days and had transient hyperbilirubinaemia. At the age of 2 months the infant showed normal development. Parvovirus infection in pregnancy is known as a cause of adverse fetal outcome, including miscarriage, fetal death, hydrops fetalis, and congenital anomalies. There have also been reports of transient pre-eclampsia-like syndromes together with fetal hydrops.3 Fetal blood transfusion has been used in cases with anaemia and hydrops. Some workers have reported spontaneous resolution of hydropsy the