Answering your questions

July 1, 2003
Edited by Daniel M. Baer, M.D.

Iodine disinfectant for infants, biohazard waste transport and stroke work-up

Iodine disinfectant for infants

In the January 2002
MLO Tips from the clinical experts, p. 25, a question was asked in regard to site preparation for infant blood cultures. In the response, a statement was made that, For patients who may be allergic to iodine compounds, chlorhexidine solutions have been shown to be exceptionally bactericidal. My questions are:

Is the chlorhexidine solution safe to use as a blood-culture prep for neonates/infants?
2. According to manufacturers, iodine has been noted as being highly absorbed and linked to hypothyroidism in the very young infant. Do you have any recommendations on using iodine on infants?
3. If these solutions are not recommended for premature and neonates, what site preparation would you recommend for blood cultures?

The Association for Womens Health, Obstetric and Neonatal Nurses and the National Association of Neonatal Nurses (AWHONN/NANN) has established a guideline on infant skin care based on a literature review published in the Journal of Obstetrical and Gynecological Neonatal Nursing.1,2 The literature review unearthed studies comparing chlorhexidine, isopropyl alcohol and povidone-iodine as skin disinfectants in adults and showed that chlorhexidine was the most effective skin disinfectant in reducing catheter-related infections. It also discovered research showing that alcohol-containing disinfectants cause the greatest amount of permanent tissue damage in study animals compared to povidone-iodine.

Finally, the literature review found evidence that when povidone-iodine compounds are used for skin disinfection, infants can demonstrate elevations in serum iodine levels, increased urinary excretion of iodine and potential systemic thyroid effects. No mention was made of the effects of chlorhexidine absorption. Keep in mind that this guideline has not yet worked itself into the phlebotomy literature or standards, but is worthy of consideration.

A study of facilities that have implemented the guideline concludes that promoting an intact skin surface may reduce systemic infection in the vulnerable neonatal population.3 Therefore, the guideline recommends chlorhexidine and povidone-iodine as skin decontaminants on neonates, but proposes that the solutions be removed with sterile saline solution or water (instead of alcohol preps) to prevent absorption. Some manufacturers of prep kits containing chlorhexidine, however, do not recommend using it on infants less than two months old, so be sure to follow the product literature accompanying any prep solution. 

Dennis J. Ernst MT(ASCP)
Center for Phlebotomy Education Inc.
Ramsey, IN


  1. Lund C, Kuller J, Lane A, Lott W, et al. Neonatal skin care: the scientific basis for practice.
    JOGNN. 1999;28(3):241-254.
  2. Alcohol Discouraged as Skin Prep on Infants.
    Phlebotomy Today 2002;3(1). Accessed June 12, 2002.
  3. Lund C, Osborne J, Kuller J, Lane A, et al. Neonatal skin care: clinical outcomes of the AWHONN/NANN evidence-based clinical practice guideline.
    JOGNN. 2001;30(1):41-51.

Biohazard waste transport

Our hospital puts specimen tubes and containers in bags (secondary containers) to transport them within the hospital. We currently use specimen bags with biohazard labels. Can labs put these specimen bags with biohazard labels into regulated waste if no contamination with blood or body fluids is visible? Do we even need to be using specimen bags with biohazard labels? I have been told that we could just use a standard Ziploc-type bag for transporting specimens within the facility and that this could be a substantial cost savings to the hospital. Could this unmarked bag be discarded in the regular trash?

Many waste facilities audit
incoming waste to be sure that biohazardous waste is not present. The presence of a biohazard labeled bag, even if clean and uncontaminated, would raise a red flag. Bags used to carry specimen containers do not need to have biohazard labels. As long as they remain clean and do not become contaminated with body fluids, they may be discarded in regular trash. This saves money, both in the lower cost of the bags and the reduction of regulated waste. In our hospital, we spend 28 cents a gallon to dispose of biohazardous waste, and approximately $75 a ton to dispose of regular trash! 

Daniel M. Baer, MD
Professor Emeritus
Department of Pathology
Oregon Health and Science University
Portland, OR

Stroke work-up

We are currently trying to
update/standardize the order sets for stroke patients. Both the ASA and another reference cite ESRs as part of the standard blood work. Why wouldnt a CRP be more appropriate? I have long been a fan of the use of CRP (Im an ancient med tech) and remember the classic paper that Dr. Nakamura published regarding use of CRP as an indicator of inflammation instead of temp, ESR or WBC and this was before the ultra-sensitive tests were available.

Both the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) should be included in the standard work-up for stroke patients. Below are the studies which support the usefulness of ESR and CRP.

  • ESR and strokes: The ESR has been shown to be a risk factor for the development of strokes.1,2,3 Also, the ESR is an independent predictor of short-term stroke outcome.3 One of the popular ESR methods is the Westergren method, which has been reported to be marginally affected by age, race and blood storage.4
  • C-reactive protein in cardiovascular diseases: CRP is an acute-phase serum protein primarily produced in the liver and is a marker for acute inflammatory response. With the development of sensitive assays for CRP,5 many studies have shown that CRP is an independent risk factor for coronary heart disease, peripheral vascular disease, atherosclerotic disease and stroke.6,7,8 The high-sensitivity CRP assay has prognostic utility in patients with acute coronary heart disease and is a strong independent predicator of future coronary events in apparently healthy persons.7
  • CRP and cerebrovascular diseases: Ford & Giles9 have reported that CRP concentration may be a risk factor or marker for stroke in the U.S. population. Other investigators have shown that an elevated CRP is a marker of increased risk in ischemic stroke10 and fatal strokes in elderly persons.11,12 The increased levels of CRP were found to be associated with a poor outcome in patients with ischemic stroke.13 Associated with elevated CRP levels in strokes, there has been reported an activation of the coagulation/fibrinolysis system14 and elevated fibrinogen levels.13

In contrast to the above reports on the value of CRP determination in strokes, Canova, et al,15 have studied 138 patients with cerebrovascular events and concluded that CRP
is not a useful marker to predict the outcome of an acute cerebrovascular event in
. Canova, et al,15 stated there was no relationship between time intervals since onset of symptoms and CRP measurement. They suggested that an acute cerebrovascular event has little influence on CRP values.

The studies by Canova and co-workers were done on patients admitted to the hospital for an acute cerebrovascular event and were prospectively studied. The Canova study15 was not designed as the other studies which determined elevated CRP as a risk factor for ischemic strokes,11,12,13 and for ischemic and fatal strokes in elderly persons.11,12
In strokes and cerebrovascular diseases, there are elevations of both CRP and ESR. Also, there is activation of the coagulation/fibrinolysis system and elevated fibrinogen levels. The ESR is influenced greatly by the levels of fibrinogen and the coagulation system.

The suggestion of adding CRP assays to the order sets for stroke patients is an excellent one. In addition, the ESR is also helpful. Each of the assays for CRP and ESR may indicate that there is deviation from the normal physiological state of the patient, such as acute inflammation or a change in coagulation system. 

Robert M. Nakamura, MD
Chairman Emeritus and Senior Consultant
Department of Pathology
Scripps Clinic
La Jolla, CA


  1. Adolfsson R, Svardsudd K, Tibblin G. 1913 men study a longitudinal study of the development of stroke in a population.
    Scand J Soc Med Suppl. 1977;14:122-127.
  2. Gillum RF, Sempos CT. Erythrocyte sedimentation rate and stroke incidence in the NHANES I Epidemiologic Follow-up Study.
    Stroke. 1997 Apr; 28(4):873-874. Comment on: Stroke. 1996 Nov; 27(11): 999-2004.
  3. Chamorro A, Vila N, Ascaso C, Saiz A, Montalvo J, Alonso P, et al. Early prediction of stroke severity. Role of the erythrocyte sedimentation rate.
    Stroke 1995 Apr; 26(40): 573-576.
  4. Saadeh C. The erythrocyte sedimentation rate: old and new clinical applications.
    South Med J. 1998 Mar; 92 (3): 220-225.
  5. Rifai N, Ridker PM. High-sensitivity C-reactive protein: a novel and promising marker of coronary heart disease.
    Clin Chem 2001 Mar; 47 (3): 403-411.
  6. Albert MA. The role of C-reactive protein in cardiovascular disease risk.
    Curr Cardiol Rep. 2000 Jul: 2 (4): 274-279.
  7. Albert MA, Ridker PM. The role of C-reactive protein in cardiovascular disease risk.
    Curr Cardiol Rep. 1999 Jul; 1 (2): 99-104.
  8. Folsom AR, Pankow JS, Tracy RP, Arnett DK, Peacock JM, Hong Y, et al. The Investigators of the NHBLI Family Heart Study. Association of C-reactive protein with markers of prevalent atherosclerotic disease.
    Am J. Cardiol. 2001 Jul 15; 88 (2): 112-117.
  9. Ford ES, Giles WH. Serum C-reactive protein and self-reported stroke: findings from the NHANES III
    Arterioscler Thromb Vasc Biol. 2000 Apr; 20_4):1052-1056.
  10. Di Napoli M, Papa F, Bocola V. C-reactive protein in ischemic stroke: an independent prognostic factor.
    Stroke 2001 Apr; 32 (4): 917-924.
  11. Gussekloo J, Schaap MC, Frolich M, Blauw GJ, Westendorp RG. C-reactive protein is a strong but nonspecific risk factor of fatal stroke in elderly persons.
    Arterioscler Thromb Vasc Biol 2000 Apr; 20(4):1047-1051.
  12. Rost NS, Wolf PA, Kase CS, Kelly-Hayes M, Silbershatz H, Massaro JM, et al. Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study.
    Stroke 2001 Nov; 32 (11):2575-2579.
  13. Di Napoli M, Papa F, Bocola V. Prognostic influence of increased C-reactive protein and fibrinogen levels in ischemic stroke.
    Stroke 2001 Jan; 32(1): 133-138.
  14. Tohgi H, Konno S, Takahashi S, Koizumi D, Kondo R, Takahashi H. Activated coagulation/fibrinolysis system and platelet function in acute thrombotic stroke patients with increased C-reactive protein levels.
    Thromb Res 2000 Dec 1: 100 (5):373-379.
  15. Canova CR, Courtin C, Reinhart WH. C-reactive protein (CRP) in cerebrovascular events.
    Atherosclerosis 1999 Nov 1: 147 (1):49-53.
Daniel M. Baer is professor emeritus of laboratory medicine at Oregon Health and Science University in Portland, OR, and a member of MLOs editorial advisory board.
MLO’s Tips from the Clinical Experts department provides
practical, up-to-date solutions to readers’ technical and clinical
issues from a panel of experts in various fields. Readers may send
questions to Dan Baer by fax, (503) 636-7932; or e-mail, [email protected].

July 2003: Vol. 35, No. 7

© 2003 Nelson Publishing, Inc. All rights reserved.