Surgical treatment of vascular trauma.
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Ten guinea pigs were irradiated with 30 Gy of x-radiation. Five were killed on the eighth day after irradiation, and the remainder were killed at the sixteenth day after irradiation. At the time of death, examination was made of the ciliary activity and the fine structure of the middle ear mucosa. Serous effusion was found in each tympanic cavity of all animals. It was shown also that the guinea pig, when irradiated with 30 Gy of x-radiation, exhibits pathologic abnormalities similar to those in humans with otitis media with effusion: degeneration of cilia or ciliated cells and changes in the vascular system (capillary injury and increased capillary permeability). Functional examinations showed that x-ray irradiation has delayed effects on ciliary activity, and the effects are much greater at the sixteenth day than at the eighth day. We speculate that the accumulation of effusion can be, at least partially, a consequence of ciliary dysfunction. The induction of sterile effusion by the use of x-ray irradiation provides a unique animal model for chronic otitis media with effusion of the serous type.
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In 144 patients on hemodialysis (76 males and 68 females, median age 55.7 +/- 14.1 years, mean period on dialysis 44.1 +/- 33.3 months), thrombomodulin was determined by enzyme immunoassay prior to initiation of hemodialysis. The results showed that the mean thrombomodulin value of hemodialysis patients was 13.59 +/- 3.63 ng/ml which was significantly higher than the control value (3.20 +/- 0.90 ng/ml). The thrombomodulin values were significantly higher in patients with blood access failure (15.27 +/- 4.45 ng/ml) than in those without (13.11 +/- 3.31 ng/ml), and the rate of blood access failures was also significantly higher in those with thrombomodulin values of 15.0 ng/ml or higher than in those with values < 15.0 ng/ml. It was evident that there is a higher risk of blood access failure in patients with severe systemic vascular endothelial injury, and thrombomodulin is a useful marker of such an injury.
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BACKGROUND: Homocysteine is involved in a complex and dynamic system of vascular injury and repair and may thus contribute to the development of diabetic microangiopathy. This still debated issue has important scientific and clinical implications, since hyperhomocysteinemia can be corrected nutritionally. AIMS: 1) To evaluate the association between fasting plasma homocysteine, type 1 diabetes and its microvascular complications; 2) to elucidate the basis of this association by investigating the major determinants of plasma homocysteine in relation to diabetic microangiopathy. METHODS: We studied sixty-six consecutive patients with type 1 diabetes mellitus of > 10 years duration and normal serum creatinine (< 115 mumol/L, 1.3 mg/dL), and free from clinically detectable cardiovascular diseases. Forty-four non-diabetic controls were also studied. Plasma concentrations of homocysteine, folate and vitamin B12 were investigated together with the C677T mutation in the gene coding for methylenetetrahydrofolate reductase (MTHFR), a key enzyme in homocysteine metabolism. Renal and retinal diabetic complications were evaluated as albumin/creatinine ratio on early-morning, urine spot collection and fundus photographs. FINDINGS: Fasting plasma homocysteine levels were very similar in patients and controls. Patients with microalbuminuria or proliferative retinopathy had significantly higher values than those without: 9.4 +/- 3.1 vs 7.4 +/- 2.8 mumol/L, p < 0.02 and 9.5 +/- 2.6 vs 7.3 +/- 3.0 mumol/L, p < 0.05. This difference was not attributable to confounders, such as age, sex and smoking, nor to dissimilar plasma folate and vitamin B12 concentrations. In contrast, homozygosity for the C677T mutation in the MTHFR gene--the commonest genetic defect linked to moderately increased plasma homocysteine--was significantly more frequent in patients with microalbuminuria and/or proliferative retinopathy (50% vs 13%, p < 0.004), odds ratio 6.7 (95% CI 1.7-27.6). CONCLUSIONS: Type 1 diabetes as such is not associated with increased plasma homocysteine levels, though patients with microalbuminuria and/or proliferative retinopathy display significantly higher values than those without. This difference is not attributable to obvious confounders, nor to differences in vitamin status, and may be partly mediated by genetic factors. Plasma homocysteine, together with other diabetes-related noxae, may thus be in a position to contribute to the development of nephropathy and the progression of retinopathy.
In 1996, 6 (7%) of 84 ulna shaft fractures treated at our institution developed compartment syndrome. These 6 isolated, comminuted, proximal-third ulna fractures were secondary to low-velocity gunshot (5) or high-velocity blunt trauma (1). The 5 gunshot-induced fractures did not initially require immediate surgical intervention, but increasing compartment pressure prompted fasciotomy and open reduction and internal fixation. The blunt trauma fracture developed compartment syndrome while the patient awaited surgery; emergent fasciotomy and open reduction and internal fixation were performed. Three patients had vascular injury (interosseus system). The orthopedist must have a high index of suspicion for compartment syndrome in association with isolated, comminuted, proximal-third ulna fractures.
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