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Biomedical subjects

T Tervo

Publications and source records attributed to T Tervo.

156 records · Page 9Linked to original sources

Fat embolism in severely injured patients.

Forty-five patients with severe blunt injuries were examined during eight posttraumatic days. At random, 14 patients were given three doses of methylprednisolone intravenously; 10 mg/kg at 8-hour intervals. Fat embolism syndrome was diagnosed in 13/45 patients, only one of whom had received corticosteroid (p = 0.03). Shock, acidosis and elevated plasma catecholamines showed no correlation with the occurrence of fat embolism syndrome. Platelet counts immediately after trauma were significantly lower in the fat embolism patients than in the other trauma patients, indicative of early platelet aggregation. Prophylactically administered methylprednisolone in pharmacological doses appeared to inhibit the emergence of fat embolism syndrome.

Embolism, Fat↗

Tear fluid cellular fibronectin levels after photorefractive keratectomy.

BACKGROUND: Fibronectin is supposed to have an important role in wound healing. The extradomain A-containing cellular fibronectin (EDAcFn) refers to fibronectin, which instead of being a hepatocyte derived component of blood plasma or body fluids, is produced locally. The present study was undertaken to clarify the possible changes in excretion of EDAcFn in tears following excimer laser photorefractive keratectomy (PRK). METHODS: An immunoassay was used to determine EDAcFn concentrations in human tear fluid samples of 11 eyes after PRK. Tear fluids were collected with scaled microcapillaries preoperatively as well as 1, 2, and 7 days after PRK. The time used to collect a known volume of tears was registered. This was done to estimate the dilution effect related to the hypersecretion of tears after PRK. RESULTS: The mean preoperative tear fluid EDAcFn concentration was 0.28 +/- 0.07 ng/microliter with a wide range (0.05 to 0.63). The tear fluid flow-corrected excretion of EDAcFn was 1.36 +/- 0.35 ng/min (range, 0.145 to 3.50). There was a significant increase in both postoperative tear fluid flow and excretion of EDAcFn on days 1 and 2. The elevation of the mean EDAcFn concentration did not decrease in spite of reflex tearing. The mean excretion of EDAcFn in tears was 28-fold on the first and 17-fold on the second postoperative day. Normal level was reached by day 7. CONCLUSION: There is a rapid increase in excretion of EDAcFn in tears following PRK. This seems to last only as long as an epithelial defect persists. The epithelium of all eyes healed in 3 to 4 days in spite of wide interindividual variations in both tear fluid flow and EDAcFn excretion.

Adult↗

Corneal wound healing and nerve morphology after excimer laser in situ keratomileusis in human eyes.

BACKGROUND: Our aim was to describe wound healing and nerve regeneration in the human cornea after excimer laser in situ keratomileusis. METHODS: Excimer laser in situ keratomileusis was done in three human eyes 8 days, 54 days, and 4 months prior to enucleation. Acetylcholinesterase reaction was used to histochemically demonstrate the corneal nerves. Immunohistochemical methods were used to demonstrate the following wound healing proteins: cellular fibronectin, tenascin, transforming growth factor-beta 1, and alpha-smooth muscle actin. RESULTS: All corneas healed without complication. No epithelial hyperplasia appeared and the Bowman's layer was smooth and acellular. An epithelial plug extending up to 100-300 microns under the flap margins was seen in all specimens. Regenerative nerve fiber bundles emerging from sharply cut anterior stromal nerves were observed, but the deeper nerves were normal. Restricted expression of fibronectin and tenascin was found at the wound area. All corneal cell types were positive for transforming growth factor-beta 1 antibody. Cells lining the limbal vessels were positive for alpha-smooth muscle actin antibody whereas the corneal cells were negative. CONCLUSIONS: The nerve morphology showed only a few abnormalities, especially in deep stromal nerves. Epithelial plugs at the flap margins may maintain a delayed wound healing process for several months but otherwise the process remained active for a relatively short time.

Acetylcholinesterase↗

Postoperative inflammation, microbial complications, and wound healing following laser in situ keratomileusis.

Although the biology of corneal wound healing is only partly understood, healing after photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK) differs in many respects, and the mechanisms appear to be differently controlled. There is less of an inflammatory and healing response after LASIK, but a longer period of sensory denervation. The cellular, molecular, and neural regulatory phenomena associated with postoperative inflammation and wound healing are likely to be involved in the adverse effects after LASIK, such as flap melt, epithelial ingrowth, and regression. Interface opacities in the early postoperative period include diffuse lamellar keratitis (DLK), microbial keratitis, epithelial cells, and interface opacities. Diffuse lamellar keratitis (sands of the Sahara syndrome) describes an apparently noninfectious diffuse interface inflammation after lamellar corneal surgery probably caused by an allergic or a toxic inflammatory reaction. Noninfectious keratitis must be distinguished from microbial keratitis to avoid aggressive management and treatment with antimicrobial drugs. Microbial keratitis is a serious complication after LASIK, but a good visual outcome can be achieved following prompt and appropriate treatment.

Cornea↗