Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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in the community too
- eliezer alkalay (4 September 2005)
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c difficile culture
- frances dockery (5 September 2005)
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Intravenous Immunoglobulin for the treatment of Clostridium Difficile Diarrhoea
- Colin J Rees, Stuart McPherson, Simon Panter (5 September 2005)
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"Prevention better than cure" - A wise man always says....
- Anand Kommuri, Ranjit K. Dhelaria (7 September 2005)
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Use of intravenous metronidazole for Clostridium difficile associated diarrhoea.
- Riaz Dor, Kalpesh Besherdas (12 September 2005)
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Is the enteral route an absolute requirement in Clostridium difficile treatment?
- Breffni C. Keegan (13 September 2005)
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Resistance of Clostridium difficile to metronidazole and vancomycin.
- Breffni C. Keegan (13 September 2005)
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Not everything that glistens is gold
- Alastair D Smith, Richard P D Cooke, Consultant Medical Microbiologist, Aintree Hospitals NHS Trust, Liverpool, L9 (18 October 2005)
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Comment on Clinical Review - Clostridium difficile associated diarrhoea: diagnosis and treatment
- Michael D Hellier (4 November 2005)
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Ciprofloxacin associated diarrhoea
- Stephen J Bromage, Stephen R. Payne (23 November 2005)
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Re: Ciprofloxacin associated diarrhoea
- Ed Cooper (24 November 2005)
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Management of Clostridium difficile in NHS Trusts
- David Green (18 January 2006)
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Clostridium Difficile and other Faecal-Oral Transmission
- J. Alastair Lack (5 February 2008)
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Comment on the recent Drug Safety Update for August 2008 published by the Medicines and Healthcare products Regulatory Agency (MHRA)
- Christopher Jones, Scott Pegler and Dr Ann M Lewis (18 August 2008)
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eliezer alkalay, rural family physician clinic of moshav herut, Israel 40691
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From the perspective of a family physician - this entity is not limited to in-hospital patients only. In a mixed-aged rural practice of about 2000 patients I have seen some cases (less than 1 in a year- diagnosis based on C. difficile toxin presence in stool), and I guess I may have misseed some more. Most of them did not need hospital, and I don't remember mortality secondary to this diagnosis in my practice. So, either not every patient with diarrhea and positive C. difficile toxin after a course of antibiotics has C. difficile associated diarrhea, OR: 1)The epidemiological statistics based on hospital diagnosis underestimate the true prevalence of the disease. 2)The description of the clinical course of the entity, including mortality rates, based on hospital-data alone, is biased towards the worst scenarios. Further study in the community is needed. Competing interests: None declared |
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frances dockery, consultant physician st. thomas's hospital london se1
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The clinical tip offered of treating culture positive, toxin negative c. difficile is contrary to the acknowledgement in the review that culture does not routinely take place in most laboratories, so this 'tip' is not applicable to current clinical practice. Competing interests: None declared |
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Colin J Rees, Consultant Gastroenterologist South Tyneside NHS Foundation Trust, Harton lane, South Shields, UK. NE34 0PL, Stuart McPherson, Simon Panter
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Dear Editor We read with interest the comprehensive review of management of Clostridium difficile diarrhoea by Starr in BMJ on September 3rd (1). A number of therapeutic options were discussed and we would like to expand upon the reference to the use of Intravenous Immunoglobulin. Patients with severe, prolonged or recurrent Clostridium difficile diarrhoea are often elderly or frail and have a poor antitoxin antibody response leading to low serum antitoxin antibodies. The use of Intravenous Immunoglobulin has been advocated in these patients(2). We have reported in abstract form the largest series of patients treated with intravenous immunoglobulin (3). This includes 10 patients, 8 responded to treatment, 2 patients died of comorbid disease. 3 patients did have recurrence of disease but all of these patients then responded quickly to conventional antibiotic treatment. All of the patients tolerated the treatment well with no side effects. Since we presented these data we have gone on to successfully treat a significant number of other patients and our protocol has been adopted by neighbouring units. This work is currently submitted for peer review publication. We would encourage consideration of the use of intravenous immunoglobulin in patients with recurrent or resistant Clostridium difficile diarrhoea in whom conventional therapy has failed, particularly in frail or elderly patients where the mortality and morbidity is high. References 1. Starr J. Clostridium difficile associated diarrhoea: diagnosis and treatment. BMJ 2005; 331: 498-501. 2. Wilcox, M. Descriptive study of intravenous immunoglobulin for the treatment of recurrent Clostridium difficile diarrhoea. Journal of Antimicrobial Chemotherapy 2004, 53, 882-884. 3. McPherson S, Rees C, Soo S, Ellis R, Panter S. Intravenous Immunoglobulin in the treatment of severe Clostridium Difficile Diarrhoea. GUT 2005; 54: A81. Competing interests: None declared |
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Anand Kommuri, Senior SHO South Tyneside Hospital, South Shields, NE34 0PL, Ranjit K. Dhelaria
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This article is very timely to address the rapid increase in incidence of C.difficile infections and I am very tempted to add our views to the problem. As the wise man always says, “ Prevention is better than cure ”, the use of antibiotics for any suspected infection has to be balanced against the higher risk of developing C.difficile infection and its associated morbidity and mortality especially in elderly. The use of antibiotics should be justified in every patient especially those who have the risk factors as mentioned by the author. Early involvement of a microbiologist and following local hospital protocols on antibiotic usage would minimise the incidence. Most often, patients attending hospital had already received a few courses of antibiotics from the primary care. A hospital microbiologist would be helpful in advising both hospital and primary care doctors for patients requiring further courses of antibiotics. Management of confirmed cases should be aggressive with special attention to barrier nursing, nutrition and early use of immunoglobulins. Immunoglobulins have been found to be effective in severe cases although a poor response is not unknown. Competing interests: None declared |
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Riaz Dor, Specialist Rergistrar in Gastroenterology Chase Farm Hospital, Enfield. Middx, EN2 8JL, Kalpesh Besherdas
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We read the review of Clostridium difficile assocaited diarrhoea with great interest ( BMJ 2005; 331: 298-501 ). However, we would disagree that metronidazole must be given by the oral route. There is clear evidence to support the use of intravenous metronidazole to successfully treat this infection. When given intravenously adequate bacteriacidal concentrations result in the stools thus making this an appropriate route of administration, particularly when there is an associated ileus, toxic colon or simply when patients cannot tolerate the oral route. References 1. Bolton RP, Culshaw MA. Faecal metronidazole concentrations during oral and intravenous therapy for antibiotic associated colitis due to Clostridium difficile. Gut, Oct 1986; 27: 1169-1172. 2. Friedenberg F, Fernandez A, Kaul V, Niami P, Levine GM. Intravenous metronidazole for the treatment of Clostridium difficile colitis. Dis Col Rectum. 2001 Aug; 44(8): 1176-80. Competing interests: None declared |
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Breffni C. Keegan, Specialist Registrar in Geriatric Medicine West Suffolk Hospital, Bury St. Edmunds, Suffolk. IP33 2QZ.
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Dear Editor Starr’s assertion that an enteral route is required for treatment1 creates difficulty for the management of those vomiting, suffering ileus secondary to Clostridium difficile, or intolerant of nasogastric tubes. It ignores prior recommendations that intravenous metronidazole be considered for those in whom an enteral route is inappropriate2, based on the pharmacokinetics of metronidazole. Oral metronidazole undergoes near complete absorption in comparison to vancomycin. It has excellent tissue penetration, and though metabolised by the liver, its main metabolite hydroxymetronidazole also possesses antibacterial properties3. When administered orally to healthy volunteers, metronidazole is reported as being undetectable in faeces, and in treatment of asymptomatic C. difficile carriers, metronidazole was detected in the faeces of only 10% of subjects4. In comparison, bactericidal faecal concentrations of metronidazole are reported in patients with C. difficile colitis receiving oral, or intravenous metronidazole. In these, levels of metronidazole and hydroxymetronidazole fell as the diarrhoea improved, and in the majority were undetectable after recovery4. The suggested mechanism to account for these findings is the secretion of metronidazole and its active metabolites into the gut lumen via inflamed colonic mucosa, though a small amount is also excreted in bile1,4. The effects of oral metronidazole on C. difficile colitis would seem accordingly, to be manifest by its systemic properties. Not surprisingly therefore that case reports, and a recent though small retrospective study5, would suggest efficacy of intravenous metronidazole in the treatment of C. difficile colitis. Whilst randomised controlled clinical trails are lacking, they appear warranted. As with oral metronidazole however, treatment failures have been reported. Nonetheless, intravenous metronidazole should be considered for the treatment of C. difficile colitis in patient groups where an enteral route is unsuitable or impracticable. References: 1.) Starr J. Clostridium difficile associated diarrhoea: diagnosis and treatment. BMJ. 2005;331(7515):498-501. 2.) Tabaqchali S, Jumaa P. Diagnosis and management of Clostridium difficile infection. BMJ. 1995;310(6991):1375-80. Review. 3.) Sweetman SC, ed. Martindale: the complete drug reference. London: Pharmaceutical Press, 2004. 4.) Johnson S, Homann SR, Bettin KM, Quick JN, Clabots CR, Peterson LR, et al. Treatment of asymptomatic Clostridium difficile carriers (faecal excretors) with vancomycin or metronidazole. A randomised, placebo-controlled trial. Ann Intern Med. 1992;117(4):297-302. 5.) Friedenberg F, Fernandez A, Kaul V, Niami P, Levine GM. Intravenous metronidazole for the treatment of clostridium difficile colitis. Dis Colon Rectum. 2001;44(8):1176-1180. Competing interests: None declared |
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Breffni C. Keegan, Specialist Registrar in Geriatric Medicine. West Suffolk Hospital, Bury St. Edmunds, Suffolk. IP33 2QZ.
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Dear Editor Starr’s assertion, that resistance in C. difficile to metronidazole and vancomycin is not reported1, is at odds with the evidence. The first case of reduced in-vitro sensitivity to metronidazole in a non-toxigenic strain of C. difficile in the UK has already been reported2, with a Minimum Inhibitory Concentration (MIC) of 16mg/L. Using British Society of Antimicrobial Chemotherapy standards, this isolate would be classified as resistant, though National Centre for Clinical Laboratory Standards would place it on the resistant breakpoint. Using data from metronidazole levels obtained in the faeces of C. difficile diarrhoea sufferers, 96% of samples had levels below the MIC for this isolate2. Though the majority of reports of reduced sensitivity of C. difficile involve non-toxigenic strains3, resistance has been described in toxigenic strains in China, France, and Spain4. Full resistance to metronidazole, and “intermediate resistance” to vancomycin were reported in the Spanish study, with higher rates among isolates from human immunodeficiency virus-infected patients3. These were not however directly linked to any treatment failures. Diagnosis nowadays, as Starr points out tends to be made by the detection of toxin, and accordingly laboratories no longer tend to culture C. difficile1. Indeed of 43,672 cases of Clostridium difficile reported to the Health Protection Agency’s Communicable Disease Surveillance Centre in 2004, <0.06% contained information on vancomycin or metronidazole sensitivity5. However, Starr’s concerns regarding delay in detecting emerging epidemic strains through failure to culture1 are currently being addressed in England through the mandatory C. difficile sampling scheme which began in January 2005, and will involve the random sampling of C. difficile for strain characterisation, from Trusts across England. Strain characterisation itself will not detect development of antibiotic resistance, but antibiotic susceptibility testing of these samples is also proposed5. References: 1.) Starr J. Clostridium difficile associated diarrhoea: diagnosis and treatment. BMJ. 2005;331(7515):498-501. 2.) Brazier JS, Fawley W, Freeman J, Wilcox MH. Reduced susceptibility of Clostridium difficile to metronidazole. J Antimicrob Chemother 2001;48:741-742. 3.) Drummond LJ, McCoubrey J, Smith DGE, Starr JM, Poxton IR. Changes in sensitivity patterns in Clostridium difficile in geriatric in-patients over an 18-month period. J Med Microbiol. 2003;52(3):259-263. 4.) Peláez T, Alcalá L, Alonso R, Rodríguez-Créixems M, García-Lechuz JM, Bouza E. Reassessment of Clostridium difficile Susceptibility to Metronidazole and Vancomycin. Antimicrob Agents Chemother. 2002;46(6):1647–1650. 5.) HPA. Voluntary reporting of Clostridium difficile, England, Wales, and Northern Ireland: 2004. Commun Dis Rep CDR Weekly [Serial online] 19 May 2005 [cited 13 September 2005] 15(20):News. Available at http://www.hpa.org.uk/cdr/archives/2005/hcai_2005.pdf. Competing interests: None declared |
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Alastair D Smith, Assistant Professor of Medicine, Division of Gastroenterology and Hepatology Rm 105, Bell Research Building, Trent Drive, Duke University Medical Center, Durham, NC 27710. USA., Richard P D Cooke, Consultant Medical Microbiologist, Aintree Hospitals NHS Trust, Liverpool, L9
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EDITOR - We appreciated Dr. Starr’s comments, but were disappointed to discover no reference to methicillin-resistant Staphylococcus aureus (MRSA) as an alternative aetiological agent for the clinical syndrome of diarrhoea and systemic upset associated with broad-spectrum anti-microbial agent exposure. 1 Although naso-pharyngeal, cutaneous and line-related colonisation with MRSA has increased steadily amongst hospital inpatients during recent years, reports of MRSA colitis in the literature remain uncommon. Nevertheless, despite being less widely appreciated than toxigenic C. difficile as a cause of nosocomial colonic infection, MRSA may result in severe and life-threatening enterocolitis. 2-4 A comparison of the risk factors and clinical circumstances in which MRSA-associated and C difficile-associated enterocolitis arise reveals that they are very similar, namely among older patients with significant co-morbid illnesses, who have been exposed to broad-spectrum anti- microbial therapy in some instances on multiple occasions, and in the setting of prolonged hospital admission and/or inter-hospital transfer. Moreover, the two organisms result in illnesses that have very similar clinical, sigmoidoscopic and histological manifestations. Thus, unless serious consideration is given to MRSA as a potential cause for diarrhoea, particularly when stool assays for C difficile toxins are negative, significant delay to diagnosis and delivery of appropriate therapy may result. It could be argued therefore, that liquid stool arising from any hospital inpatient should be analyzed for MRSA, not least as an effective infection control measure. References: 1. Starr J. Clostridium difficile associated diarrhoea: diagnosis and treatment. (Review: 31 references) BMJ 2005;331:498-501. 2. Taylor M, Ajayi F, Almond M. Enterocolitis caused by methicillin- resistant Staphylococcus aureus. Lancet 1993;342:804. 3. Smith AD, O’Bierne JPJ, Cooke RPD. Methicillin-resistant Staphylococcus -aureus associated colitis, a potentially life threatening illness may present with a number of features similar to Clostridium difficile associated colitis (abstract). Am J Gastroenterol 2002;97:S198-S199. 4. Rhee KY, Soave R, Maltz C. Methicillin-resistant Staphylococcus aureus as a cause of antibiotic-associated diarrhea. J Clin Gastroenterol 2004;38:299-300. 5. Bignardi GE. Risk factors for Clostridium difficile infection. J Hosp Infect 1998;40:1-5. Competing interests: None declared |
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Michael D Hellier, Consultant Physician/Gastroenterologist The Great Western Hospital, Swindon & Marlborough NHS Trust, SN3 6BB
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There is one glaring omission in this otherwise admirable account of a very important and increasing clinical problem. Pseudomembranous colitis, the most serious complication of C.difficile infection, gets but half a paragraph with no comment on its management. Pseudomembranous colitis is probably responsible for the majority of deaths from this gastrointestinal infection and can lead to fulminating colitis not unlike that seen in non-specific inflammatory bowel disease. It needs to be recognised early and treated aggressively. Much of the morbidity and mortality stemming from C.difficile infection relates to delay in diagnosis. Patients suffer diarrhoea in hospital which is often attributed to antibiotics but not investigated appropriately. It is of the utmost importance that those patients particularly at risk - the elderly, those who have had antibiotics and post orthopaedic surgery patients - are referred early for a specialist gastroenterological opinion where diarrhoea is persisting. Pseudomembranous colitis can only be diagnosed by examining the lower bowel and by taking biopsies for histology. The message must be, think early of the diagnosis and seek specialist gastroenterological advice. Competing interests: None declared |
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Stephen J Bromage, research fellow Manchester Royal Infirmary, M139WL, Stephen R. Payne
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Antibiotic associated diarrhoea is a common problem with hospital inpatients and, as discussed in a recent review article, can be due to a Clostridium Difficile infection [1]. Ciprofloxacin is perhaps the most commonly prescribed antibiotic in urological practice. It has an excellent spectrum of activity against organisms responsible for urinary tract infections, yet may be associated with diarrhoea in up to 8% of patients [2]. We were concerned that, in our practice, diarrhoea was occurring in >8% of our patients treated with ciprofloxacin so we set up a prospective audit to determine the exact proportions and causative factors for diarrhoea associated with this antibiotic. We looked at 105 inpatients prescribed oral antibiotics, of whom 89 received ciprofloxacin. There were no episodes of diarrhoea in the 16 patients prescribed other oral antibiotics, but loose stools occurred in 26% of those prescribed ciprofloxacin. 39% of these patients experienced such severe diarrhoea that they discontinued the course of ciprofloxacin. Those inpatients with ciprofloxacin associated diarrhoea underwent stool culture. One patient had clostridium associated diarrhoea, but had been prescribed other intravenous antibiotics that increased the risk. There were no other positive stool cultures. There have been recent reports of growing resistance to ciprofloxacin, with organisms such as e.coli [3] and it is, therefore, important that any course of ciprofloxacin should be completed. Our experience suggests that diarrhoea is much more common than expected in association with ciprofloxacin and often leads to truncation of the prescribed course. There have been many mechanisms implicated in this antibiotic associated diarrhoea, such as disturbed composition and function of intestinal flora, or direct pro- kinetic effect, rather than clostridial infection. Therefore, we should be considering treatment of this diarrhoea with an anti-motility drug, such as loperamide, when ciprofloxacin has been prescribed in isolation. References 1. John Starr. Clostridium difficile associated diarrhoea: diagnosis and treatment. BMJ 2005; 331: 498-501. 2. Ball P. Ciprofloxacin: an overview of adverse experiences. J Antimicrob Chemother. 1986 Nov;18 Suppl D:187-93. Review. 3. Barisic Z, Borzic E, Kraljevic KS, Carev M, Zoranic V, Kaliterna V. Rise in ciprofloxacin resistance in Escherichia coli from urinary tract infections from 1999-2004. Int J Antimicrob Agents. 2005 Jun;25(6):550-1 Competing interests: None declared |
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Ed Cooper, Locum Cons. Pediatrician London
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Stephen Bromage and Stephen Payne, in their response, say: "There have been recent reports of growing resistance to ciprofloxacin ... and it is, therefore, important that any course of ciprofloxacin should be completed". This seems to revert to an old idea, that organisms are more likely to become resistant when antibiotic courses are curtailed. This does not fit natural selection, which holds that a variant that is fitter under selection pressure will reproduce more successfully. The longer the selection pressure is applied, the more successful the resistant variant will be. The allelic gene of this variant is likely to be present before the selection pressure is applied, but only to reproduce successfully in comparison with other ("wild-type") alleles during the pressure period. Therefore the shorter a course of antibiotic, the less likely the development of resistance. Excessively short courses of antibiotics spare some of the organisms, which can then go on to reproduce and cause a flare-up of the disease; but if they were sensitive before then they will still be sensitive. Competing interests: None declared |
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David Green, Lead Nurse Infection Control Bradford Royal Infirmary, Duckworth Lane, Bradford, BD9 6RJ
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Dear Sir, A recent report and press statement by the Healthcare Commission and Health Protection Agency1, 2 that a third of NHS Trusts are failing to adhere to “government guidance” on the prevention and control of Clostridium difficile infection gives cause for concern. In parallel the Chief Medical Officer and the Chief Nursing Officer have written a joint letter to trust chief executives3. The letter states that guidance published in 1994 by the Department of Health and the then Public Health Laboratory Service4 (now the Health Protection Agency) is “current”. I telephoned the publication department of the DH for a copy only to be told they do not have anything that goes back “that far”, a similar request to the HPA also drew a blank. Oddly this same guidance that is said to be “current” does not appear in the report1 as a standard against which trusts have been measured. The HC and HPA report1 advises trusts have antibiotic prescribing guidelines to reduce the risk of Clostridium difficile infection. However the supporting reference given was a report made to rather than guidance from the Department of Health. The report was in fact the findings of the National Clostridium difficile Standards Group5, an expert group “established at the request of the DH to review evidence pertaining to the diagnosis and control of” Clostridium difficile associated diarrhoea and to “make recommendations for the development of the surveillance system”. This group made a number of recommendations to the DH but despite their report being nearly 3 years old and surveillance now in place, there has been no updated guidance on prevention and control. One wonders what guidance it is that trusts are not adhering to and whose advice should be followed in the future. The press release from the Healthcare Commission and HPA2 focuses exclusively on the negative findings of the report1 and sadly findings that “89% of trusts have a written policy that covers the management of infection from C. difficile” have therefore gone unreported in the media. If trusts are to reduce the incidence of infection from Clostridium difficile it is my opinion that a useful starting point is guidance contained in a single document that is both current and accessible. Yours sincerely David Green
References 1. Health Protection Agency/Healthcare Commission, Management, prevention and surveillance of Clostridium difficile: Interim findings from a national survey of NHS acute trusts in England, 21st December 2005. http://www.hpa.org.uk/infections/topics_az/clostridium_difficile/InterimReport05.pdf 2. Healthcare Commission Press Release, Healthcare agencies urge the NHS to step up measures to minimise risk of patients contracting Clostridium difficile. 21st December 2005http://www.healthcarecommission.org.uk/NewsAndEvents/PressReleases/PressReleaseDetail/fs/en?CONTENT_ID=4022047&chk=n0pJM/ 3. Chief Medical Officer and Chief Nursing Officer’s Letter, infection caused by Clostridium difficile. PL CMO/2005/6; PLCNO2005/5, 21st December 2005. 4. Clostridium difficile infection: Prevention and Management. A Report by a Department of Health/PHLS joint working group. BAPS Health Publications Unit, Heywood Manchester 1994 5. National Clostridium Standards, Report to the Department of Health, February 2003 Competing interests: None declared |
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J. Alastair Lack, Consultant Salisbury SP5 4LX
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There is a fundamental flaw in our attempts to interrupt the path of faecal-oral transmission of pathogens. The typical lavatory cubicle in most public areas, including many hospitals, will contain only a pan and a roll of paper. After the toilet paper has been used, clothing is replaced with potentially contaminated hands, transmitting pathogens to clothing and cubicle lock before the washbasin (usually outside) is used. Thereby clothing, lock and washbasin taps are contaminated, and so on to other members of the community. It is surely appropriate to provide in lavatories, complementing the toilet paper, a hand sterilising gel that can be used before replacing clothing. Competing interests: None declared |
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Christopher Jones, Trust Antibiotics Pharmacist Morriston Hospital, ABM University NHS Trust, Swansea, SA6 6NL, Scott Pegler and Dr Ann M Lewis
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Dear Sir/Madam, We wish to comment on the recent Drug Safety Update for August 20081 published by the Medicines and Healthcare products Regulatory Agency (MHRA), and in particular, the guidance "Metronidazole for Clostridium difficile associated diarrhoea: use oral formulation”. The Drug Safety Update states that “Only the oral formulation of metronidazole should be used for this indication (Clostridium difficile associated diarrhoea (CDAD)), unless advised otherwise (in exceptional cases) by specialists in the treatment of CDAD." We believe the statement may cause confusion and possible sub-optimal treatment of CDAD by suggesting that the use of intravenous metronidazole in CDAD is exceptional. Intravenous metronidazole is indicated in CDAD in severe to fulminant cases. Intravenous administration bypasses the frequently encountered complication of ileus and negates the significant delay in drug delivery from the stomach to the colon as a result of delayed gastric emptying. Faecal concentrations of metronidazole are within the therapeutic range via this route owing to biliary excretion and increased exudation across the intestinal mucosa during CDAD2. Intravenous metronidazole is also appropriate for patients requiring therapy for CDAD who are nil by mouth. Indeed, draft guidance from the Steering Group on Healthcare Associated Infection “Clostridium difficile Infection: How to Deal with the Problem a Board to Ward Approach” endorses the above3. We believe that ‘erroneous’ prescribing of intravenous medication can occur with all drugs, not just with metronidazole, and should call for greater care and attention when prescribing and administering all medication. However, the use of metronidazole as described above has been used out of context, leading to the misleading statement made in the Drug Safety Update. References: 1. Drug Safety Update. Volume 2, Issue 1 August 2008 from MHRA and CHM. Accessed from www.mhra.gov.uk/Publications/Safetyguidance/DrugSafetyUpdate/index.htm on 4/8/2008. 2. Bolton, RP, Culshaw, MA. Faecal metronidazole concentrations during oral and intravenous therapy for antibiotic associated colitis due to Clostridium difficile. Gut 1986;1169. 3.Clostridium difficile Infection: How to Deal with the Problem A Board to Ward Approach. A report to the Department of Health from the Steering Group on Healthcare Associated Infection. ( Draft for Comment) Authors: Christopher Jones, Trust Antibiotics Pharmacist, Scott Pegler, Principal Pharmacist, Medicines Information Manager Dr Ann M Lewis, Consultant Medical Microbiologist Morriston Hospital, ABM University NHS Trust, Swansea, SA6 6NL Competing interests: None declared |
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