Biomedical subjects
Publications and source records attributed to F J Manahan.
We performed acute peritoneal dialysis on eight end-stage renal disease patients using a bicarbonate-containing solution sterilized by ultrafiltration through polyamide filters. The patients tolerated the procedure well; their azotemia and metabolic acidosis improved.
Superoxide produced by neutrophils plays an important role in the killing of bacterial pathogens. The effects of glucose-containing peritoneal dialysis solutions on superoxide production by canine and human neutrophils were studied. A significant decrement in superoxide generation was noted with the 2.27% and 3.86% glucose solutions. The results suggest that hypertonic peritoneal dialysis solutions curtail neutrophil superoxide generation.
Neutrophils were isolated from canine blood and exposed to a conventional, acidic, lactate-containing peritoneal dialysis solution for 0, 2 and 4 minutes in one study and 0, 4, 7 and 10 minutes in another. Superoxide generation, expressed in nanomoles per million cells, was determined using a method based on the superoxide dismutase-inhibitable reduction of ferricytochrome c. Brief exposure of neutrophils to a conventional dialysis solution could significantly inhibit the generation of superoxide by neutrophils.
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Human neutrophils were isolated from healthy volunteers and exposed to either bicarbonate-containing (pH 7.4) or lactate-containing (pH 5.2) peritoneal dialysis solution in vitro. Superoxide production by neutrophils was measured by a method based on the superoxide dismutase-inhibitable reduction of ferricytochrome c. Bicarbonate-containing peritoneal dialysis solution was found to be superior to the lactate-containing one in facilitating the production of superoxide anion by human neutrophils.
We evaluated the feasibility of using L-lactate as a base for hemodialysis. In one study, acid-base changes using 40 mM L- or DL-lactate were compared. In a second study, acid-base status using various amounts of L-lactate exclusively was studied. The third study compared symptoms and acid-base changes during 9 weeks of high-efficiency dialysis when using L-lactate, acetate, or bicarbonate as base. In the first study, plasma bicarbonate changes were equivalent with 40 mM L-lactate and 40 mM DL-lactate, but overall correction of acidosis appeared to be suboptimal. In the second study, when compared to a bicarbonate control period, correction of acidosis was reduced when using 40 mM L-lactate + 4 mM acetate solution, but increased when using a 46 mM L-lactate + 4 mM acetate solution. In the third study, correction of acidosis was comparable when using 42 mM L-lactate + 4 mM acetate, 39 mM acetate, or 35 mM HCO3 + 4 mM acetate. Whereas 46% +/- 12 (SEM) treatments "failed" because of symptoms when using acetate, the percentages of "failed" treatments were only 7% +/- 4.2 with L-lactate (p less than 0.05) and 11% +/- 4.2 with bicarbonate (p less than 0.05). The results suggest that L-lactate is a suitable dialysis solution base that is capable of correcting chronic uremic acidosis. During high-efficiency dialysis, the incidence of intradialytic symptoms with L-lactate is comparable to that with bicarbonate and less than that with acetate.
The formula -In (R - 0.03 - UF/W), where R is the ratio of the postdialysis to predialysis plasma urea nitrogen level, UF the ultrafiltrate volume per session, and W the postdialysis weight, has been shown by us to estimate K.t/V accurately. We audited the amount of dialysis being administered in a moderate size outpatient unit in which urea kinetic modeling was not being done and in which 4 hr dialysis at a 250 or 300 ml/min blood flow rate was routinely prescribed. R was determined once per month on each of six successive months, and standard three point urea kinetic modeling was done on all patients once. R was quite reproducible in each patient, with a coefficient of variation of 6.6% +/- 3.2 standard deviation (SD). The R:UF:W-derived K.t/V averaged 0.91 +/- 0.19; the R:UF:W-derived K.t/V correlated with the modeled K.t/V (r = 0.98), with a mean percent error of only 0.12% +/- 3.6. A negative correlation (r = -0.56) was present between the R:UF:W-derived K.t/V and postdialysis weight; 9 of 40 patients had K.t/V values below 0.8 and 7 of these 9 weighed more than 85 kg. In 13 other patients, K.t/V was between 0.8 and 0.9. After inclusion of residual renal function (Kru) to calculate KT, KT was still below 0.9 in 19 patients. The main cause of underdialysis was inadequate prescription. The results suggest that monthly monitoring of R, with inclusion of UF and W to estimate K.t/V, is one useful quality assurance tool to assess the amount of dialysis being administered.
This case study describes an atypical case of refractory, sodium warfarin-induced necrotizing fasciitis and myonecrosis. This patient did not initially receive surgical debridement and systemic antibiotics, the standard treatment for necrotizing fasciitis of bacterial origin. This patient's wound care regimen began with silver sulfadiazine and wet-to-dry dressings, modified to initial cleansing with a zinc-saline solution, followed with application of a zinc-saline wet dressing, impregnated with an aluminum hydroxide ointment. The patient experienced pain relief after the first application. After 4 weeks, the necrotic tissue sloughed off, the early signs of healing appeared making surgical debridement possible. Therapy with the zinc-saline dressings was continued and restoration of all tissues was documented within 225 days. If aggressive surgical therapy is not an option, the prevention of secondary complications such as infection becomes the goal of treatment until the necrotic process stops and healing begins. For this goal, a moist environment may be the optimal choice for topical therapy.