To study the epidemiology -especially the impact of contaminated stopcocks -on central venous catheter (CVC) infection and catheter-related sepsis (CRS), semiquantitative (SQ) and quantitative (Q) culture methods and typing of coagulase-negative staphylococci (CNS) were employed in 49 neonates with clinical signs of sepsis while receiving parenteral nutrition in the paediatric intensive care unit. The patients were divided into two groups according to stopcock contamination: group A consisted of 18 patients (36%) with contaminated stopcocks and group B consisted of 31 patients (64%) with sterile stopcocks. Five specimens were obtained from each patient, in addition to that from the stopcock: a swab taken from the skin surrounding the catheter puncture site; the CVC tip; the intradermal segment (IDC); and samples of parenteral fluid and blood. A total of 294 specimens (392 sites) was cultured and micro-organisms were identified. All CNS isolated were typed by biotyping, antibiogram, plasmid analysis and pulsed-field gel electrophoresis (PFGE), and the discriminatory power of the typing methods was compared. The CVC tips were infected in 25 patients (51%); 15 (83%) in group A and 10 (32%) in group B. Sepsis was detected in 24 neonates (@YO), 13 in group A and 11 in group B. This was catheter-related in 15 patients (63%), 12 in group A and 3 in group B. CNS were recovered from 13 (52%) of 25 infected CVCs, nine in group A and four in group B. Sixty-five CNS isolates were recovered from these patients and belonged to 14 biotypes, 22 antibiograms, 22 plasmid profiles and 26 PFGE types. Typing showed that in six of nine patients in group A, CNS of the same type were recovered from the catheter tip and the stopcock, in one patient the catheter tip and skin isolates were the same and in two others the catheter tip isolates were different from stopcock and skin isolates. In all four patients in group B, different CNS types were recovered from CVC tips and skin. Bacteraemia was caused by CNS in 14 patients (58%), six in group A and eight in group B. v p i n g confirmed that nine cases (six in group A and three in group B) were catheter-related but five were not. SQ and Q culture methods and typing, especially by PFGE, allowed the study to determine that bacteria from contaminated stopcocks were frequently the source of CVC infection and CRS.

The objective of our study was to present our experience in the treatment of small children with continuous renal replacement therapy (CRRT) and plasma exchange (PE). From March 1986 to April 2000, 21 critically ill children (14 newborns and 7 infants) with acute renal failure (ARF) and multiple organ failure were treated with CRRT and PE. In the newborn group, there were 8 males and 6 females, age 15.7 +/- 11.7 days, with body weights of 3,348 +/- 585 g. In the infant group, there were 4 males and 3 females, age 118 +/- 67 days, with body weights 5,186 +/- 734 g. The indications for the beginning of CRRT and/or PE were ARF with anuria and hyperhydration (17 patients), azotemia and anuria (1 patient), hemolytic uremic syndrome (1 patient), and hyperammonemia (2 patients). In all patients, peritoneal dialysis was considered inappropriate. PE and CRRT monitors were used, double lumen 5 Fr and 7 Fr hemodialysis catheters were the vascular access, low dose heparin and prostacyclin were anticoagulants, and lactate or bicarbonate buffered replacement solutions were used predilutionally. Side events were clotting within the extracorporeal circuit, catheter malfunction, serious hypotension (6 patients), and pulmonary edema (1 patient). Ten of 21 patients (47.6%) recovered renal function and 9 of 21 patients (42.9%) survived. Survivors had fewer failing organs (3.6 +/- 0.5) than nonsurvivors (4.8 +/- 0.9) (p = 0.0008). Pump driven CRRT and PE were feasible, efficient, and safe procedures in newborns and infants. Without CRRT, it is uncertain whether any of our patients would have the chance to survive.

Key words child, naloxone, poisoning, respiratory insufficiency, tramadol.Tramadol therapy has gained wide popularity in the last few years, not only with regard to cancer patients on chronic pain therapy, but also in other acute or chronic pain problems. It is an atypical analgesic, which is contraindicated in infants below 1 year of age. Tramadol has a dual mechanism of analgesic action. It inhibits re-uptake of norepinephrine and serotonin, in addition to m-opioid receptors agonism. The former action is mostly due to the parent compound tramadol, while its metabolite O-demethyltramadol (M1) exerts its primary action at the m-opioid receptor. 1-5 Tramadol metabolite M1 is mainly formed by genetically polymorphic cytochrome P450 (CYP) 2D6. In extensive CYP2D6 metabolizers the analgesic effects of tramadol are superior to those in poor metabolizers. 1 Unintentional intoxication with severe central nervous system (CNS) depression and seizures has been reported in small children. 6-8 We report a case of tramadol intoxication in which treatment with naloxone was diagnostic and therapeutic. Case reportA 4-year-old girl with no recent history of acute illnesses, but with a past history of catheter dilatation of a stenotic pulmonary artery and vesico-ureteric reflux grade II, was admitted to a regional hospital because of irregular breathing, cyanosis, respiratory depression, somnolence, and shaking of the whole body after she fell asleep. Before sleeping she was playing in her grandparents' living room. On admission at 17.20 hours to the general hospital she was febrile (38.8°C), with a sore throat. She was cyanotic, tachycardic (160 beats/min), and had a blood pressure of 104/ 65 mmHg, and a systolic murmur of stenotic pulmonary artery was heard. She was bradypnoeic, with a respiratory rate of 16/min. She looked frightened and agitated but initially responded adequately to the usual social questions. During examination she became more frightened and started hallucinating (seeing something on the shaking floor). Twenty minutes after admission she had a tonic-clonic seizure lasting 1 min that was self-limiting without therapy. Afterwards, she remained opistotonic and somnolent. One hour later she started to react to painful stimuli and, despite constricted pupils, protected her eyes from light. An evaluation for sepsis was performed. Results of a complete blood count, serum electrolytes including glucose, urinalysis, urine culture, blood culture and cerebrospinal fluid culture were normal. Blood gas analysis indicated respiratory acidosis and desaturation (exact values of venous blood gases were: pH, 7.12; pCO2, 10.04 kPa; pO2, 3.88 kPa; base excess, -5.8 mmol/L; HCO3 -, 23.9 mmol/L; total CO2, 26.2 mmol/L), pulse oxymetry reading on air was between 77% and 79%, so she was placed in an oxygen tent. Electrocardiogram showed right-sided hypertrophy. One hour later she had a second tonic-clonic seizure, which was again self-limiting, therefore no anticonvulsant therapy was given. Urgent computed tomography (CT) of the bra...

Children with normal and low CI were differentiated by T-lymphocytes and HLA-DR+ monocytes. Since no differences in methylprednisolone exposure and cortisol plasma levels between the low-CI and normal-CI groups were found, it can be concluded that factors other than methylprednisolone must contribute to differences in the cell-mediated response.

Very few data exist on phosphate metabolism in critically ill neonates. Therefore we studied the incidence of hypophosphataemia, the intracellular metabolism of phosphate by measuring adenosine 5'-triphosphate (ATP) and 2,3-diphosphoglycerate (2,3-DPG) in red blood cells, and excretion of phosphate in urine. The aims of the study were early detection of changes in phosphate metabolism as possible diagnostic markers of sepsis and defining the cause of hypophosphataemia. Neonates, treated in multidisciplinary paediatric intensive care unit (PICU), included in the study, were less than three days of age. Eighteen of them had respiratory distress syndrome (RDS) and 16 had microbiologically confirmed or clinical sepsis. The overall incidence of hypophosphataemia in critically ill neonates was over 80%, and was more common (88%) and more profound in those with sepsis than in those with RDS (79%). Therefore the septic neonates needed significantly larger amounts of phosphate to maintain normophosphataemia. In septic neonates ATP concentration in red blood cells was significantly lower than in neonates with RDS and controls, while the 2,3-DPG concentration was increased as a result of compensation. In septic neonates urinary losses of inorganic phosphate (Pi) were significantly higher than in neonates with RDS. Hypophosphataemia in critically ill neonates is at least partly due to higher urinary losses of phosphate.