[Bacterial contamination of salvaged blood in open heart surgery: is that an airborne contamination or a normal skin flora contamination?].

We investigated sources of bacterial contamination of intraoperative salvaged blood producted by autologous transfusions device (CS; CELL SAVER 5, Heamonetics Corp., Braintree, MA). Eleven patients undergone open heart surgeries including 2 emergency operations with a median sternotomy enrolled in this study. Blood samples were drawn from salvaged blood bags. Airborne contaminants (AB) were collected by a blood agar plate put besides the operation bed for 30 minutes. The median wounds samples were collected by a swab. Bacterial growth was detected in 81.8% of salvaged blood samples. Twenty-nine bacterium were isolated from CS, 72.4% of those were Staphylococci. 9.1% of sample was positive in wound swabs. Forty bacterium were isolated from plate cultures. 65% of them were Staphylococci. Staphylococcus epidermidis and coagulase negative Staphylococcus isolated both CS and AB in the 2 cases had the same identify codes, and incubated from several AB cultures. Corynebacterium sp. is also isolated from both CS and AB cultures in other 2 same cases. In 7 out of 8 cases (87.5%), from which Staphylococci isolated in CS, the Staphylococci were cultured from AB in not the same but the other cases. In conclusion, highly incidence of the identification in identical code of Staphylococci indicated that the main source of CS contamination was highly suspected to AB.

Multicenter clinical trial for evaluating methylprednisolone pulse treatment of idiopathic optic neuritis in Japan. Optic Neuritis Treatment Trial Multicenter Cooperative Research Group (ONMRG).

BACKGROUND: A randomized, controlled clinical trial was conducted in 1991 to compare an intravenous megadose of methylprednisolone with a control drug (mecobalamin) for treating acute idiopathic optic neuritis. CASES: Sixty-six cases from 22 clinical centers throughout Japan were examined to evaluate the treatment on visual function parameters, such as visual acuity, visual field, color vision, contrast sensitivity, and critical flicker frequency. OBSERVATIONS: The methylprednisolone pulse treatment group showed faster recovery of visual function, particularly the visual acuity at 1 week (P<.05), Humphrey field analyzer mean deviation at 3 weeks (P<.05), and color vision at 1 week (P<.05). Recovery of contrast sensitivity at several different spatial frequencies was significant in the pulse treatment group at 1 (P<.01), 2 (P<.05), and 4 weeks (P<.05) after the start of treatment. Visual function test results at 12 weeks and 1 year were essentially the same in the two treatment groups. Side effects appeared more frequently in the pulse treatment group than in the control (P<.05). CONCLUSIONS: Pulse treatment does not appear effective for idiopathic optic neuritis even though visual function in the pulse treatment group of this trial recovered more quickly during the initial phase compared to the controls. More effective and specific treatment should be established for optic neuritis.

Neonatal intrahepatic cholestasis with hepatic siderosis and steatosis.

Neonatal intrahepatic cholestasis is a heterogeneous disease of undetermined cause. There is an unreported subset of idiopathic neonatal intrahepatic cholestasis with an unusual histological combination of hepatic siderosis and macrovesicular steatosis. The patients were a 34-day-old female and a 39-day-old male with normal birth weights. Their mothers had received oral iron supplement 4-6 weeks before delivery. The patients had obstructive jaundice noticed at the well-baby clinic at 1 month of life. They had high levels of serum galactose and tyrosine, hyperferritinemia. Urinary organic acid and bile acid analyses were negative, and galactose-1-phosphate uridyltransferase activity in red cells was normal. Liver biopsies showed diffuse iron deposits and macrovesicular fat. By substituting formula milk with lactose-free milk, the patients responded, and had normal biochemical tests within 5 months of life. Follow-up biopsies, at the age of 12 months, showed mild residual fibrosis without iron or fat deposits. They are both well at 3 and 6 years of age, respectively, without biochemical liver dysfunction and neurologic impairment. Prenatal iron-overload might contribute to the pathogenesis of the disease, but further studies are needed to confirm the assumption.

Subclinical liver dysfunction in one-month-old infants with a low activity of vitamin K dependent coagulant factors assessed by normotest.

To clarify features of late vitamin K deficiency hemorrhagic disease in Japanese infants, seventeen of 1,687 infants screened by normotests were examined for signs and symptoms suggesting hepatobiliary diseases. Clinical observations disclosed findings suggesting hepatobiliary diseases in 7 of the 17 selected infants with normotest values of less than 40%, and 11 infants had abnormal results in one or more liver function tests. Taken together, 14 of the 17 infants had findings suggesting hepatobiliary diseases. Upon vitamin K supplementation normotest values improved in various degrees in all infants, whether or not they had signs or symptoms of hepatobiliary diseases. Late vitamin K deficiency hemorrhagic disease of infancy may be related to subclinical hepatobiliary diseases.

Evaluation of the nutritional condition and absorptive capacity of nine infants with short bowel syndrome.

Nutritional conditions and absorptive capacity of nine infants with short bowel syndrome were investigated during a long follow-up period from 1.5 years to 14 years and 7 months. The length of the residual small intestine ranged between 13-90 cm. The nine infants had normal meals at home and most of them did not suffer from persistent diarrhea. Most of the infants were thin. Nutritional parameters were kept relatively normal. The results of D-xylose absorption test had gradually improved, but the absorptive capacity of sugars and amino acids, observed by potential differences, were within the normal limits or slightly subnormal except for one infant. This indicated that the absorptive capacity of sugars and amino acids per a given area of the residual small intestine did not increase. Severe steatorrhea continued for several years in infants with less than 50 cm of small intestine. In these infants the concentration of serum vitamin D and total cholesterol were below the normal limits and the absorption of bile acids was disrupted. From our examination, infants with less than 50 cm of small intestine must be followed up for a long period and nutritional supplements are necessary.

Serum vitamin E levels in children with corrected biliary atresia.

In 37 children with long-standing cholestasis who had undergone a Kasai's procedure (double Roux-en-Y hepatic portoenterostomy), serum vitamin E levels were determined. In addition, serum bile acid levels were simultaneously tested as a marker of cholestasis. Eighteen of 37 children had vitamin E levels of less than 0.50 mg/100 ml, and two showed neurological abnormalities including hypoactive deep tendon reflexes and ataxia. Serum vitamin E levels were inversely correlated with serum bile acid levels (p less than 0.01). Older patients have mild cholestasis and high serum vitamin E levels in comparison with younger ones. Improvement in bile excretion into the intestinal tract with age seemed to be responsible for an increase of serum vitamin E levels. Oral supplements of alpha-tocopherol in doses of 5 to 10 mg/kg/day were needed to maintain the normal serum vitamin E levels in postoperative infants.

Familial intrahepatic cholestasis associated with progressive neuromuscular disease and vitamin E deficiency.

Three Japanese patients with familial progressive intrahepatic cholestasis developed complications involving neurologic abnormalities characterized by ataxia and pigmentary retinopathy. Serum vitamin E concentrations were extremely low in all patients, suggesting a long-term vitamin E deficiency. High dose oral supplementation of alpha-tocopherol produced normal serum vitamin E levels in two patients. Parenteral administration of vitamin E resulted in no clinical improvement in one patient who first received the treatment at 14 years of age. In the other two patients, the progression of neurological abnormalities was slowed by vitamin E supplementation. Cholestyramine treatment resulted in an apparent decrease in serum vitamin E levels despite oral alpha-tocopherol supplementation.