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(1/977) Anterior instability of the glenohumeral joint with humeral avulsion of the glenohumeral ligament. A review of 41 cases.

We studied retrospectively a consecutive series of 547 shoulders in 529 patients undergoing operation for instability. In 41, the cause of instability was considered to be lateral avulsion of the capsule, including the inferior glenohumeral ligament, from the neck of the humerus, the HAGL lesion. In 35, the lesion was found at first exploration, whereas in six it was noted at revision of a previous failed procedure. In both groups, the patients were older on average than those with instability from other causes. Of the primary cases, in 33 (94.3%) the cause of the first dislocation was a violent injury; six (17.4%) had evidence of damage to the rotator cuff and/or the subscapularis. Only four (11.4%) had a Bankart lesion. In patients undergoing a primary operation in whom the cause of the first dislocation was a violent injury, who did not have a Bankart lesion and had no suggestion of multidirectional laxity, the incidence of HAGL was 39%.  (+info)

(2/977) Extradural inflammation associated with annular tears: demonstration with gadolinium-enhanced lumbar spine MRI.

Annular tears are manifest on MRI as the high-intensity zone (HIZ) or as annular enhancement. Patients with annular tears may experience low back pain with radiation into the lower limb in the absence of nerve root compression. Inflammation of nerve roots from leak of degenerative nuclear material through full-thickness annular tears is a proposed mechanism for such leg pain. The aim of this study is to illustrate the appearance of extradural enhancement adjacent to annular tears in patients being investigated for low back pain with radiation into the lower limb(s). Sagittal T1- and T2-weighted spin echo and axial T1-weighted spin echo sequences were obtained in eight patients being investigated for low back and leg pain. In all patients, the T1-weighted sequences were repeated following intravenous gadopentetate dimeglumine (Gd-DTPA). Annular tears were identified at 12 sites in eight patients. Extradural inflammation appeared as a region of intermediate signal intensity replacing the fat between the posterior disc margin and the theca, which enhanced following Gd-DTPA. The inflammatory change was always associated with an annular tear, and in four cases directly involved the nerve root. Enhancement of the nerve root was seen in two cases. The findings may be relevant in the diagnosis of chemical radiculopathy secondary to inflammation at the site of an annular leak from a degenerating disc.  (+info)

(3/977) Sonographic incidence of tendon microtears in athletes with chronic Achilles tendinosis.

OBJECTIVE: To assess the number and distribution of tendon microtears in asymptomatic controls and athletes with chronic Achilles tendinitis or partial thickness tears using high resolution ultrasound. METHODS: The mean number of microtears in three random tendon cross sections were recorded per tendon third in 19 asymptomatic volunteers, 16 athletes with symptomatic chronic Achilles tendinitis, and eight athletes with partial Achilles tendon rupture. RESULTS: Microtears were most numerous in the middle third section of the Achilles tendon. Some 67% of tendons in the control group had no microtears, and 28% showed a single microtear. Only 18% of the athletes with chronic Achilles tendinitis and none of the athletes with partial tendon rupture were without microtears in the middle third of their Achilles tendon. Of the tendons with chronic tendinitis, 13% had more than three microtears per section which increased to 87% in tendons exhibiting partial rupture. CONCLUSIONS: There appears to be an association between microtear formation and Achilles tendon rupture.  (+info)

(4/977) Traumatic wound rupture after penetrating keratoplasty in Africa.

AIM: To investigate risk factors, visual outcome, and graft survival for traumatic wound rupture after penetrating keratoplasty. METHODS: A retrospective analysis of 336 patients who underwent penetrating keratoplasty from 1988 to 1995. RESULTS: 19 patients (5.7%) suffered traumatic postoperative wound rupture requiring surgical repair. They were younger (mean age 16.6 years, 95% CI 13.2-20.6) and more frequently keratoconic (p = 0.01) than other patients (mean age 28.9 years, 95% CI 26.-31.0). Mean postoperative follow up was 37.7 (SD 22.9) months and 24.5 (18.9) months for the rupture and non-rupture patients. Mean interval between keratoplasty and rupture was 18 (21) weeks. The lens was damaged and removed in 37% of ruptured eyes. For keratoconics, the probability of graft survival at 5 years was lower (p = 0.03) in the ruptured eyes (75%) than in the non-ruptured eyes (90%). Endothelial failure was a more common (p <0.05) cause of graft opacification in ruptured grafts than in intact grafts. Of the ruptured eyes, 53% achieved a final corrected acuity of at least 6/18 and 63% achieved at least 6/60 compared with 48% and 71% of the intact eyes respectively (both p >0.1). The proportion of keratoconic eyes which achieved at least 6/60 was lower (p = 0.02) in the ruptured eyes (67%) than the non-ruptured eyes (87%). Eyes with wound ruptures of 5 clock hours or greater were less likely (p <0.05) to achieve an acuity of 6/18 and were more likely (p <0.05) to have an associated lens injury. CONCLUSIONS: Graft rupture is relatively common in African practice, particularly in young keratoconics. Visual outcome and graft survival are not significantly worse than for other grafted eyes, but are significantly worse than for other grafted keratoconic eyes.  (+info)

(5/977) Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques.

BACKGROUND: Several recent studies attempted to classify plaques as those prone to cause clinical manifestations (vulnerable, atheromatous plaques) or those less frequently associated with acute thrombotic complication (stable, fibrous plaques). Defining the cellular and molecular mechanisms that underlie these morphological features remains a challenge. Because interstitial forms of collagen determine the biomechanical strength of the atherosclerotic lesion, this study investigated expression of the collagen-degrading matrix metalloproteinase (MMP) interstitial collagenase-3 (MMP-13) and the previously studied MMP-1 in human atheroma and used a novel technique to test the hypothesis that collagenolysis in atheromatous lesions exceeds that in fibrous human atherosclerotic lesions. METHODS AND RESULTS: Human carotid atherosclerotic plaques, similar in size, were separated by conventional morphological characteristics into fibrous (n=10) and atheromatous (n=10) lesions. Immunohistochemical and Western blot analysis demonstrated increased levels of MMP-1 and MMP-13 in atheromatous versus fibrous plaques. In addition, collagenase-cleaved type I collagen, demonstrated by a novel cleavage-specific antibody, colocalized with MMP-1- and MMP-13-positive macrophages. Macrophages, rather than endothelial or smooth muscle cells, expressed MMP-13 and MMP-1 on stimulation in vitro. Furthermore, Western blot analysis demonstrated loss of interstitial collagen type I and increased collagenolysis in atheromatous versus fibrous lesions. Finally, atheromatous plaques contained higher levels of proinflammatory cytokines, activators of MMPs. CONCLUSIONS: This report demonstrates that atheromatous rather than fibrous plaques might be prone to rupture due to increased collagenolysis associated with macrophages, probably mediated by the interstitial collagenases MMP-1 and MMP-13.  (+info)

(6/977) Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction.

BACKGROUND: Rupture of the fibrous cap of an atherosclerotic plaque is a key event that predisposes to acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) may contribute to weakening of the cap, which favors rupture. Stromelysin, a member of MMP family, is identified extensively in human coronary atherosclerotic lesions. It can degrade most of the constituents of extracellular matrix as well as activating other MMPs, which suggests that it may play an important role in plaque rupture. Recently, a common variant (5A/6A) in the promoter of the stromelysin gene has been identified. The 5A/6A polymorphism could regulate the transcription of the stromelysin gene in an allele-specific manner. METHODS AND RESULTS: To investigate the relation between the 5A/6A polymorphism in the promoter of the stromelysin gene and AMI, we conducted a case-control study of 330 AMI patients and 330 control subjects. The prevalence of the 5A/6A+5A/5A genotype was significantly more frequent in the patients with AMI than in control subjects (48.8% vs 32.7%, P<0.0001). In logistic regression models, the odds ratio of the 5A/6A+5A/5A was 2.25 (95% CI, 1.51 to 3.35). The association of 5A/6A polymorphism with AMI was statistically significant and independent of other risk factors. CONCLUSIONS: The 5A/6A polymorphism in the promoter of the stromelysin gene is a novel pathogenetic risk factor for AMI.  (+info)

(7/977) Ocular explosion during cataract surgery: a clinical, histopathological, experimental, and biophysical study.

INTRODUCTION: An increasing number of cases are being recognized in which a peribulbar anesthetic for cataract surgery has been inadvertently injected directly into the globe under high pressure until the globe ruptures or explodes. We reviewed the records of 6 such cases (one of which was reported previously by us), and one additional case has been reported in the literature. Surprisingly, 2 of these 7 cases went unrecognized at the time, and the surgeons proceeded with the cataract operation; all of the patients ultimately developed severe visual loss and/or loss of the eye. OBJECTIVES: To reproduce this eye explosion in a live anesthetized rabbit model and to perform a clinical, histopathological, experimental, biophysical, and mathematical analysis of this injury. METHODS: Eyes of live anesthetized rabbits were ruptured by means of the injection of saline directly into the globe under high pressure. The clinical and pathological findings of the ruptured human and animal eyes were documented photographically and/or histopathologically. An experimental, biophysical, and mathematical analysis of the pressures and forces required to rupture the globe via direct injection using human cadavers, human eye-bank eyes, and classic physics and ophthalmic formulas was performed. The laws of Bernoulli, LaPlace, Friedenwald, and Pascal were applied to the theoretical and experimental models of this phenomenon. RESULTS: The clinical and pathological findings of scleral rupture, retinal detachment, vitreous hemorrhage, and lens extrusion were observed. In the exploded human and rabbit eyes, the scleral ruptures appeared at the equator, the limbal area, or the posterior pole. In 2 of the 7 human eyes, the anterior segments appeared entirely normal despite the rupture, and cataract surgery was completed; surgery was canceled in the other 4 cases. In 4 of the 5 injected and ruptured rabbit eyes, the anterior segments appeared essentially normal. The experiments with human eye-bank eyes and the theoretical analyses of this entity show that the pressure required to produce such an injury is much more easily obtained with a 3- or 5-mL syringe than with a syringe 10 mL or larger. CONCLUSIONS: Explosion of an eyeball during the injection of anesthesia for ocular surgery is a devastating injury that may go unrecognized. The probability of an ocular explosion can be minimized by careful use of a syringe 10 mL or larger with a blunt needle, by discontinuing the injection if resistance is met, and by inspecting the globe prior to ocular massage or placement of a Honan balloon. When ocular explosion occurs, immediate referral to and intervention by a vitreoretinal surgeon is optimal. Practicing ophthalmologists should be aware of this blinding but preventable complication of ocular surgery.  (+info)

(8/977) Recurrent carotid blowout syndrome: diagnostic and therapeutic challenges in a newly recognized subgroup of patients.

BACKGROUND AND PURPOSE: To our knowledge, recurrent carotid blowout syndrome (rCBS) has not been well described. Our purpose was to review our institution's recent experience with patients who presented with multiple episodes of carotid blowout syndrome (CBS), and who were referred for emergent diagnostic angiography and endovascular therapy. METHODS: We retrospectively reviewed the last 46 consecutive patients who had a clinical diagnosis of CBS. All patients were examined and treated prospectively according to a standardized protocol. Most patients (43 of 46) had undergone extensive primary and salvage radical surgery with intraoperative brachytherapy or external beam radiation or both. The remaining three patients had either traumatic or iatrogenic CBS. RESULTS: Twelve patients (26%) in our series had more than one episode of CBS in which a total of 32 (20 recurrent) events were observed (average 2.7, range 2-4). Intervals of rCBS ranged from 1 day to 6 years. Thirteen (65%) of 20 recurrent events were attributed to progressive disease (PD), and seven (35%) of 20 to treatment failures (TFs). In the PD group, seven (54%) of 13 had recurrent ipsilateral disease, and six (46%) of 13 had recurrent contralateral disease. Etiologies of rCBS were as follows: seven exposed carotids; seven carotid pseudoaneurysms; eight small-branch pseudoaneurysms; five tumor hemorrhages; three hyperemic/ulcerated wounds; and one aortic arch rupture. Twenty-seven of 32 events were treated with endovascular therapy, which included the following: nine carotid occlusions; 11 small-branch embolizations; three transarterial tumor embolizations; one carotid stent; and two direct-puncture embolizations. Four of six TFs were retreated successfully with endovascular therapy; the remaining two TFs were managed successfully by surgery. In the PD group, hemorrhagic complications of rCBS were managed successfully in all but one patient, who died. No permanent neurologic or ophthalmologic complications occurred. CONCLUSION: Recurrent CBS is a frequently encountered problem in which most cases are caused by PD resulting from both multifocal iatrogenic arteriopathy and occasional wound complications that are characteristic of aggressively managed head and neck surgical patients. Initial TFs are encountered often as well. Despite the diagnostic and therapeutic challenges of rCBS, most cases can be retreated effectively.  (+info)