1193

started, initially using a haemofilter with a membrane area of 0.015 m2 (Amicon ’Minifilter’), as recommended for this age, with cannulation of the femoral artery and vein (gauge 22). However, the ultrafiltration rate was not sufficient to lower the ammonia

widespread use of ciprofloxacin for non-travellers’ diarrhoea3 until the importance of these findings is known.

concentration, which increased to 885 umol/1. A 0.2 m2 haemofilter (Amicon ’Diafilter-10’) was substituted, and the arteriovenous

Sheffield S10 2JF. UK, and Department of Experimental and Clinical Microbiology, Medical School, University of Sheffield

catheter system shortened to decrease extracorporal blood volume. Ammonia and glutamine concentrations decreased to normal within ten hours (ammonia 46 Nmol/1, glutamine 235 flII1o1jl), ammonia clearance being 5 ml/min per m2. The child strikingly improved within two days, recovering from the metabolic crisis without residual neurological defects, and continues to develop normally at 3 months of age. CAVH in combination with specific conservative measures is an effective, simple, and widely applicable method for management of acute metabolic crisis due to hyperammonaemia in newborn babies. Therapy can be initiated rapidly, involves a much smaller extracorporeal volume than haemodialysis, and is better tolerated by haemodynarnically unstable patients. CAVH can be modified by the length and diameter of the arteriovenous line, the surface areas of the filters, by prefilter and postfilter dilution, and by negative pressure at the ultrafiltrate outlet.3 Few complications related to continuous anticoagulation or vascular access are associated with CAVH.44 W. SPERL R. GEIGER H. MAURER J. P. GUGGENBICHLER

Department of Paediatrics, University of Innsbruck, A-6020 Innsbruck, Austria

Department of Bacteriology, Royal Hallamshire Hospital,

C. J. BATES M. H. WILCOX R. C. SPENCER D. M. HARRIS

1. Johnson S, Clarbots CR, Linn FV, Olson NM, Peterson LR, Girding DN. Nosocomial Clostridium difficile colonisation and disease. Lancet 1990; 336: 97-100. 2. Viscidi R, Willey S, Bartlett JG. Isolation rates and toxigenic potential of Clostridium difficile isolates from various patient populations. Gastroenterology 1981; 81: 5-9. 3. Editorial. Quinolones in acute non-travellers’ diarrhoea. Lancet 1990; 336: 282.

Is anti-HCV blood donor screening useful? van der Poel and colleagues (March 10, p 558) report than 5000 blood product transfusions. All 6 anti-HCVpositive units implicated in non-A, non-B hepatitis (NANBH) cases also had raised ALT values, and the 9 "seroconversions" without hepatitis were, according to van der Poel et al (July 21, p 187), non-specific. If these observations prove representative, the sensitivity of anti-HCV screening of ALT screened donor blood would be about zero.

SIR,-Dr

more

Red Cross Blood Service,

North-Rhine-Westphalia, D-4400 Muenster, Germany

** This letter has been shown whose reply follows.-ED. L.

H. FIEDLER

to

Dr

van

der Poel and

colleagues,

1. Donn

SM, Swartz RD, Thoene JG. Companson of exchange transfusion, peritoneal dialysis, and haemodialysis for the treatment of hyperammonaemia in an anunc newborn infant. J Pediatr 1979; 95: 67-70. 2. Wiegand C, Thompson T, Bock GH, Mathis RK, Kjellstrand CM, Mauer SM. The management of life-threatening hyperammonemia: a comparison of several therapeutic modalities. J Pediatr 1980; 96: 142-44. 3. Zobel G, Trop M, Ring E. Arteriovenous haemofiltration in hypervolaemia. Arch Dis Child 1986; 61: 803-04. 4 Lieberman KV. Continuous arteriovenous haemofiltration

m

children. Pediatr

Nephrol 1987; 1: 330-38.

Ciprofloxacin and Clostridium difficile infection SIR,-Dr Cain and Dr O’Conner (Oct 13, p 946) describe a case of

pseudomembranous colitis after treatment with ciprofloxacin. We have observed two cases of superinfection with Clostridium difficile during treatment with ciprofloxacin. Both patients had symptomatic enteric salmonellosis due to Salmonella virchow and received ciprofloxacin 500 mg twice daily for 7 days. In the first case was initiated because of pyrexia in an immunocompromised patient with an underlying lymphoma. The other patient had profuse diarrhoea and continued to excrete

treatment

salmonella 2 weeks after the first isolation and was treated to reduce the risk of cross-infection. Both patients became symptom-free while on treatment, but day 7 faecal samples were found to contain C difficile toxin. Neither patient was excreting C difficile toxin before treatment. Ciprofloxacin was discontinued immediately and C difficile toxin was not detectable in follow-up specimens. These cases are further evidence of the potential of treatment with ciprofloxacin to result in superinfection with C difficile. A study of symptom-free excretors of C difficile has shown that such patients may not be at increased risk of diarrhoea.1 However, the presence of faecal C difficile toxin is a more specific finding in symptomatic adult patients than isolation of the organism alone.2 Both of our patients were excreting C difficile toxin yet remained well. Although the importance of these fmdings is uncertain, we feel that symptomless patients should not be ignored because complications may develop later and because they may represent a source of cross-infection. Examination of follow-up faecal specimens for C difficile toxin is probably not often done. In the light of these reports of C difficile superinfection it may be wise to do this in ciprofloxacin-treated individuals. Caution should be exercised with regard to the

SjR,—Dr Fielder asks whether screening for antibodies to hepatitis C virus (HCV) in donor blood, already tested within normal ranges for alanine aminotransferase (ALT), would be of increased sensitivity for the prevention of post-transfusion non-A, non-B hepatitis (PTH-NANB). Indeed, the data we reported do not contradict Fiedler’s statement. By retesting of recipients with HCV-RNA polymerase chain reaction (PCR)l in 1990, we found that one without PTH-NANB but who had seroconverted (ELISA) in 1984-86 was PCR positive. This recipient had received HCV-positive blood (C100-ELISA and RIBA) that nevertheless had a normal ALT. The donor of the implicated blood product also transmitted HCV on other occasions (van der Poel CL, et al, unpublished). This shows that anti-HCVpositive on C100-ELISA, but ALT normal, donor blood can transmit HCV. Despite the low numbers of our recipients with PTH-NANB, these findings are supported by those of other prospective studies. Alter et aP reported that only 4/12 (33%) anti-HCV (C100-ELISA) positive blood transfusions, implicated in PTH-NANB, had raised ALT levels. Esteban et al3 reported a sensitivity for PTH-NANB of 3/13 (23%) for recipients receiving blood with raised ALT, as opposed to 14/25 (56%) for recipients of blood positive for anti-HCV on C 100 ELISA. Moreover, introduction of surrogate testing for ALT and anti-HBc during the course of this study did not significantly reduce the incidence of PTH-NANB. One might therefore reverse Fiedler’s question: is ALT screening of blood donors for the prevention of PTH-NANB still useful, now that a more specific assay with at least a comparable1 or even better,3 sensitivity is at hand? Red Cross Blood Bank Amsterdam, 1066 CX Amsterdam, Netherlands

C. L. VAN DER POEL H. W. REESINK

Central Laboratory of the Red Cross, Blood Transfusion Service, Amsterdam

H. TH. M. CUYPERS P. N. LELIE W. SCHAASBERG

AJ, Kuo G, Bradley DW, et al. Detection of hepatitis C viral sequences in non-A, non-B hepatitis. Lancet 1990; 335: 1-3. 2. Alter HJ, Purcell RH, Shih JW, et al. Detection of antibody to hepatitis C virus in prospectively followed transfusion recipients with acute and chronic non-A, non-B hepatitis. N Engl J Med 1989; 321: 1494-500. 3. Esteban JI, Gonzalez A, Hernandez JM, et al. Evaluation of antibodies to hepatitis C virus in a study of transfusion-associated hepatitis. N Engl J Med 1990; 323: 1. Weiner

1107-12.