Contamination of pulse oximeter probes before and after decontamination in two intensive care units.

Background: The internal surfaces of pulse oximeter probes may be overlooked as hot spots for pathogenic microorganisms in an intensive care unit (ICU), thereby contributing to the high incidence of hospital-acquired infections. Objectives: To determine the growth and identification of microorganisms on pulse oximeter probes in the multidisciplinary ICU (MICU) at Charlotte Maxeke Johannesburg Academic Hospital and the burns ICU (BICU) at Chris Hani Baragwanath Academic Hospital, before and after decontamination. Methods: This was a cross-sectional, comparative and contextual study, using purposive sampling. Data were collected from the internal surfaces of 34 pulse oximeter probes in a MICU and BICU. Each pulse oximeter probe was swabbed before and after decontamination. The endemic microorganism profile for the two ICUs was obtained from a laboratory database. Results: Internal surfaces of 31 (91%; 95% confidence interval (CI) 0.76 - 0.98) pulse oximeter probes were contaminated with 9 different pathogenic microorganisms pre decontamination. Acinetobacter baumannii, Klebsiella pneumoniaei and Pseudomonas aeruginosa were endemic to both ICUs, and were the most-frequently isolated microorganisms. Staphylococcus aureus was the most common microorganism endemic to both ICUs, isolated on the internal surfaces of only 2 pulse oximeter probes. Of the internal surfaces of pulse oximeter probes, 6 (18%; 95% CI 0.07 - 0.35) remained contaminated post decontamination, with a microorganism growth reduction of 80% (p=0.0001). Conclusion: The internal surfaces of pulse oximeter probes may serve as hot spots for an array of pathogens with the potential to cause infection and outbreaks in ICUs. Decontamination of the internal surfaces of pulse oximeter probes should be emphasised. Contributions of the study: This study identifies internal surfaces of pulse oximeter probes as reservoirs for infection in intensive care units (ICUs), particularly in a burns ICU setting, pinpointing one of many sources of hospital-acquired infections within ICU cubicles.The study emphasises the need to clean the internal surfaces of pulse oximeter probes (whether visibly soiled or not) prior to disinfection.

Contamination of pulse oximeter probes before and after decontamination in two intensive care units

Background. The internal surfaces of pulse oximeter probes may be overlooked as hot spots for pathogenic microorganisms in an intensive care unit (ICU), thereby contributing to the high incidence of hospital-acquired infections. Objectives. To determine the growth and identification of microorganisms on pulse oximeter probes in the multidisciplinary ICU (MICU) at Charlotte Maxeke Johannesburg Academic Hospital and the burns ICU (BICU) at Chris Hani Baragwanath Academic Hospital, before and after decontamination. Methods. This was a cross-sectional, comparative and contextual study, using purposive sampling. Data were collected from the internal surfaces of 34 pulse oximeter probes in a MICU and BICU. Each pulse oximeter probe was swabbed before and after decontamination. The endemic microorganism profile for the two ICUs was obtained from a laboratory database. Results. Internal surfaces of 31 (91%; 95% confidence interval (CI) 0.76 - 0.98) pulse oximeter probes were contaminated with 9 different pathogenic microorganisms pre decontamination. Acinetobacter baumannii, Klebsiella pneumoniae and Pseudomonas aeruginosa were endemic to both ICUs, and were the most-frequently isolated microorganisms. Staphylococcus aureus was the most common microorganism endemic to both ICUs, isolated on the internal surfaces of only 2 pulse oximeter probes. Of the internal surfaces of pulse oximeter probes, 6 (18%; 95% CI 0.07 - 0.35) remained contaminated post decontamination, with a microorganism growth reduction of 80% (p=0.0001). Conclusion. The internal surfaces of pulse oximeter probes may serve as hot spots for an array of pathogens with the potential to cause infection and outbreaks in ICUs. Decontamination of the internal surfaces of pulse oximeter probes should be emphasised

Nephron-sparing surgery for bilateral wilms' tumours: a single-centre experience with 23 cases

Introduction: The challenge of management with bilateral Wilms' tumours is the eradication of the neoplasm; while at the same time preserving renal function. Surgical management with a variety of nephron-sparing techniques; combined with chemotherapy and occasionally supplemented by transplantation has evolved over the last 30 years to achieve remarkable success. We document the experience of a single centre in a developing country. Material and Methods: Twenty-three bilateral Wilms' tumours were seen in our service between 1981 and 2007. Treatment was; in most cases; according to National Wilms' Tumour Study Group protocols; with initial bilateral biopsy; neoadjuvant chemotherapy; and tumourectomy. Technique of nephrectomy included full mobilization of the tumour-involved kidney; topical cooling with slush ice; vascular exclusion; tumour resection and reconstruction of the remnant kidney. Results: Twelve patients are alive and free of disease one to 15 years after treatment; all with well-preserved renal function (lowest glomerular filtration rate was 65 ml/min per (1.73 m 2 ). None of the survivors have hypertension. Eleven have died (two of unrelated disease) including six of the seven with spread outside the kidney. All three with unfavourable histology are alive. Four of the five metachronous presentations are alive; as are eight of 12 patients with synchronous bilateral tumours who presented since 2000. Conclusions: Appropriate chemotherapy and nephron-sparing surgery can achieve good results with preservation of adequate renal function in nearly all cases. Unfavourable histology did not have a reduced survival in our series. Metastatic spread outside the kidney had a poor prognosis

Melatonin protects against alterations in hippocampal cholinergic system, trace metals and oxidative stress induced by gestational and lactational exposure to cadmium.

Dietary exposure to cadmium, even at lower doses, can lead to free radical induced neurotoxicity, neurobehavioral changes and alteration in neurotransmitters. Such changes are likely to be more pronounced in the developing brain due to incompleteness of blood brain barrier (BBB). Hippocampus being the seat of intelligence has a role in learning and cognitive behavior and any damage to hippocampus during developmental stage is likely to result in neurodegenerative changes in later life. To this end, fetal and neonatal exposure to cadmium was induced by exposing pregnant dams of Swiss albino strain throughout the period of gestation and following parturition up till 5th day post partum (pp) through drinking water (3ppm/animal/day). The neonates were sacrificed on day 6 pp and indices of oxidative stress, levels of trace elements and changes in cholinergic system were evaluated in the hippocampus. Increased lipid peroxidation, surge in reactive oxygen species (ROS), depressed antioxidant defense, increased accumulation of cadmium, differential alterations in trace elements and decreased activity of AChE were the features of cadmium toxicity. Simultaneous administration of melatonin to cadmium challenged animals offset these detrimental changes. The results suggest that melatonin co-administration can effectively protect against the adverse effects of cadmium on endogenous antioxidant status, changes in trace metal concentrations and compromised hippocampal cholinergic system.

Presentation and outcome of 25 cases of Fanconi's anemia.

Twenty-five children with Fanconi's anemia (FA) who attended the Paediatric Haematology Clinic of Red Cross Children's Hospital over the past 20 years were retrospectively reviewed. There was a female predominance with 17 girls and 8 boys in the group. The clinical features and laboratory data are enumerated. An unusually high prevalence of gastrointestinal anomalies (20%) was found. Seventeen children received an adequate trial of androgen therapy and in 12 the initial hemoglobin concentration increased by more than 2 g/dl or return to normal. Most patients subsequently required intermittent courses of androgens but three were able to stop treatment and maintain a normal hemoglobin concentration for from 3.5 to 20 years. Ten patients remain alive, of whom five had less severe hematological problems and did not require any treatment. The mean period of follow-up of the survivors is 8.7 years. Thirteen patients have died, with a mean time of 5.5 years from diagnosis to death. Of the deaths, two were due to malignant disease and one resulted from cerebral hemorrhage. The other 10 children died of confirmed or suspected infections. Treatment options of FA are discussed.

Toxicokinetics and bioavailability of oral and intravenous 1,1-dichloroethylene.

Although aliphatic halocarbons have been identified as contaminants of drinking water supplies, little definitive information is available on their gastrointestinal (G.I) absorption and toxicokinetics. Therefore, a study of a representative halocarbon, 1,1-dichloroethylene (1,1-DCE), was undertaken to contrast the kinetics of the chemical following iv injection with that following oral administration. Four dosage-levels of 1,1-DCE (10, 25, 50, and 100 mg/kg BW) in 50% aqueous polyethylene glycol 400 were given iv and po to fasted and nonfasted male Sprague-Dawley rats. Serial blood samples were taken from the tail artery of the lightly etherized animals for up to 490 min after dosing. 1,1-DCE concentrations in the whole blood were determined by gas chromatographic head-space analysis. Evaluation of the iv data revealed that disappearance of 1,1-DCE from the systemic circulation followed a triexponential pattern. Light ether anesthesia did not appear to alter the pharmacokinetics of iv-injected 1,1-DCE. There was no difference between nonfasted and fasted iv rats in biological half-life (t1/2) or in any other pharmacokinetic parameter. Total body clearance, t1/2, apparent volume of distribution and volume of distribution in the central compartment did show increases with increasing dose in these animals. Oral dosing experiments revealed that 1,1-DCE was absorbed very rapidly and completely from the G.I. tract. Peak blood levels were reached 2 to 8 min following oral administration of 1,1-DCE as an aqueous suspension. The t1/2 of 1,1-DCE in orally dosed rats was somewhat longer than in their iv counterparts. The t1/2 values for nonfasted, orally dosed rats were longer than for their fasted counterparts, suggesting delayed absorption due to the presence of food in the G.I. tract. Bioavailability of 1,1-DCE, as determined by comparing areas under blood concentration versus time curves (AUCs), was equivalent in animals given the same dose of 1,1-DCE iv and po. AUCs increased with increasing dose in iv and po groups, but the increases were not proportional to dose.