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Long-Term Venous Access in Leukæmia

1980, The Lancet

1412 TABLE II-RESPONSE OF CORNEAL XEROPHTHALMIA TO SYSTEMIC VITAMIN A IN CHILDREN WITH PROTEIN-ENERGY I I I I MALNUTRITION* I *Defined as one or more of the following: serum albumin <3.0 or transferrin <50 mg/dl; weight for height <70% of standard; cedema. g/dl pedal These results are hardly surprising. Severe xerophthalmia requires the virtual absence of holo-retinol-binding protein (holo-RBP, the physiologically active form of the vitamin) from the serum.’ Healthy children absorb 70-80% of a massive oral dose of vitamin A.2 Since 200 000 IU is 7 times the total vitamin A stores of a well nourished 7.5 kg child,3 even markedly reduced absorption is compatible with assimilation of clinically significant amounts of the vitamin. Differences in serum "vitamin A" response to massive dosing should not be confused with the relative adequacy of the amounts absorbed. Most of this "vitamin A" is in the form of inactive ester. Despite a marked difference in the serum "vitamin A" level of oral and intramuscular recipients in our study, their holo-RBP responses were virtually identical.’ Even these were probably in excess of clinical requirements: corneal healing among cases of protein-energy malnutrition was rapid (if not always sustained) (table n) despite an intimate relationship between holoRBP response and protein status (to be published). Since children with diarrhoea are at increased risk of xerophthahriia, any method for increasing their vitamin A intake should be investigated. Just because absorption of orally administered vitamin A is reduced does not necessarily mean it is "unwise" to add vitamin A to oral rehydration fluid. If enough can be provided, sufficient amounts may be absorbed to prevent severe xerophthalmia. There is nothing new in the concept that reduced absorption may be overcome by larger doses, as commonly observed in other malabsorptive states.4 Wilmer Ophthalmologic Institute, Johns Hopkins Hospital, Baltimore, Maryland 21205, U.S.A. A. SOMMER catheters placed.’ The series has now been extended to 51 adult acute leukaemia patients who have had 67 catheters (8 Broviac, 59 Hickman) placed since September, 1977. The patients have received standard intensive induction therapeutic regimens2 or one of a variety of regimens for patients in relapse.3.4 The catheter was used for blood drawing and for administration of multiple antibiotics, antifungal agents, intravenous push medications, electrolyte solutions, and all blood products (platelets, red and white blood cells). Catheters have been in place for a median 7 weeks (range 0.5to 84), with a median 8 weeks (range 0.5 to 69); the patients were outpatients, and the catheter was cared for by family and patient. All patients were granulocytopenic with neutrophil counts of less than 300/&micro;1 for a median of 3 weeks (range 1-17 weeks). In contrast to the 6/25 catheters that Blacklock et al. removed because they had clotted, only 4 of the 59 Hickman catheters in our series have needed to be removed for clots. They were in place a median of 3.5months at the time of the clot. The use of heparin flush (800 U) given whenever blood passed in or out of the line (e.g., with blood product transfusion, blood drawing, or blood backflow into the line) plus the use of a continuous infusion pump to ensure that fluid is continuously passing through the catheter when it is not capped may explain our lower frequency of this complication. Blacklock et al. record a 56% frequency for catheter exit site infection; we have had no exit site infections. We do not use sodium hypochlorite solution to clean the catheter when it is disconnected. We do use a strict aseptic dressing change and skin cleansing technique to the exit site area every 48 h. The exit site area is first scrubbed with acetone to defat the skin and help prevent fungal superinfection. This is followed by a saline rinse, then a 2 min 2% iodine scrub, and application of efferdine ointment to the exit site itself. After this, a sterile occlusive dressing is placed. There were four insertion site infections (6%), one necessitating catheter removal. Only one catheter tip itself was proven infected (2%) and that catheter was in a vessel that had become clotted in association with disseminated intravascular coagulation. One additional tip was highly suspicious. Both of these were Staphylococcus epidermidis infections and both cleared after catheter removal and antibiotics. Of the remaining 13 catheters that had been removed in outpatients, and the 16 catheters that were inspected at necropsy, neither the catheters nor any of the vessels or the heart appeared in any way abnormal. In 20 patients who died and on whom no necropsy was done there had been no ante-mortem indication of infection. This is despite a 67% frequency of septicoemia, with an additional 6 patients who had disseminated Candida and 6 patients who had invasive Aspergillus infection found post mortem. We have found that the catheter has become a key element in the supportive care of the acute leukarmia patients. There is very low complication rate associated, when the constant infusion pump and careful dressing change technique are used. Departments of Medicine, Surgery, and Nursing, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, U.S.A. JANET ABRAHM JAMES MULLEN NANCY JACOBSON ROSEMARY POLOMANO LONG-TERM VENOUS ACCESS IN LEUK&AElig;MIA SIR,&mdash;Dr Blacklock and colleagues (May 10,. p. 993) describe the use of a modified right atrial catheter for venous access in leukaemia patients. We have a more extensive and different experience with such catheters. Our first report described 25 patients with adult acute leukaemia who had 32 1. Abrahm J, Mullen JL, Jacobson N, Polomano R. Continuous central venous access in patients with acute leukemia. Cancer Treat Rep 1979; 63: 2099-2100. 2. Cassileth PA, Katz ME. Chemotherapy for adult acute nonlymphocytic leukemia with daunorubicin and cytosine arabinoside. Cancer Treat Rep 1977; 66: 1441-45. JA, Wiernik PH. A comparative clinical trial of 5-azacytidine and 3. Levi 2. Kusin JA, Reddy V, Sivakumar B. Vitamin E supplements and the absorption of a massive dose of vitamin A. Am Clin Nutr 1974; 27: 774-76. 3. Pirie A. Effect of vitamin A deficiency on the cornea. Trans Ophthalmol Soc UK 1978; 98: 357-60. RM, Smith VC, Multack R, Krill AE, Rosenberg IH. Dark-adap- 4. Russel testing for diagnosis of subclinical vitamin-A deficiency and of therapy. Lancet 1973; ii: 1161-63. tation tion evalua- in previously treated adults with acute nonlymphocytic leukemia. Cancer 1976; 38: 36-41. 4. Whitecar JP, Bodey GP, Freireich EJ et al. Cyclophosphamide vincristine (NSC-26271), (NSC-67574), cytosine arabinoside (NSC-63878), and prednisone (NSC-10023) (COAP) combination chemotherapy for acute leukemia in adults. Cancer Chemother Rep 1972; 56: 543-50. guanazole