The three-dimensional anatomy of proximal humeral fractures.

HYPOTHESIS: Three-dimensional (3D) computed tomography (CT) reconstructions have the potential to convey the anatomy of proximal humeral fractures more realistically than do standard 2D images. MATERIAL AND METHODS: Proximal humeral fractures in 248 adult patients were examined prospectively using 3D CT reconstructions. To our knowledge, this represents the largest reported series of such fractures examined by this method. RESULTS: Of 248 fractures examined by a 3D classification system, 14% were of the 2 Part type, 36% were 3 Part, 21% were Shield fractures, 13% were isolated tuberosity injuries, and 16% were fracture dislocations. CONCLUSIONS: This study led to a modification of the Neer classification system. The frequency of each type of injury in this new classification is presented and a technique for viewing 3D images is suggested which maximizes their usefulness. LEVEL OF EVIDENCE: Level 2; Clinical, observational, and prospective.

Natural history of complex fractures of the proximal humerus using a three-dimensional classification system.

We studied the nonoperative treatment of proximal humeral fractures in severe injuries usually treated surgically. The natural history of 63 patients was followed prospectively for 2 to 9 years (mean, 42 months) with a nonrandomized protocol. A 3-dimensional classification system based on computed tomography scans was used to categorize the fractures. Assessment was made for range of motion, function via a validated testing instrument (Simple Shoulder Test), analog pain score, avascular necrosis (AVN), and fracture union. Magnetic resonance imaging for early signs of AVN was done in 16 cases. After conservative treatment of complex fractures of the shoulder, motion is considerably compromised but pain is minimal and functional status is acceptable to most individuals in this predominantly older patient population. Status comparable to a successful surgical shoulder fusion is achieved in most cases-Nature's fusion. Contrary to common belief, AVN, even in severely displaced injuries, is rare. Future randomized studies based on a 3-dimensional classification need to be done to compare these natural history results with various types of surgical interventions.

Periodontal care may improve endothelial function.

BACKGROUND: Periodontitis is a chronic, infectious, insidious disease of the tooth-supporting structures that causes a general inflammatory response. The aims of this study were to determine whether periodontitis is associated with endothelial dysfunction leading to cardiovascular events and whether proper management of periodontal disease would improve endothelial function and prevent cardiovascular events in the future. METHODS: Twenty-two patients (12 women, 10 men; 40+/-5 years old) took part in the study. All had severe periodontitis (without systemic disorders) and were all treated conservatively. Thirteen patients returned for a second visit after 3 months of treatment. Endothelial function and periodontal status were evaluated on entry into the study and 3 months following treatment. Ten age-matched, healthy volunteers without periodontal disease served as the control group. RESULTS: There was a significant difference between the patient group and the healthy controls: FMD% 4.12+/-3.96 vs. 16.60+/-7.86% (p=0.0000). Periodontitis improved significantly in all 13 patients who completed 3 months of treatment, and their endothelial function improved as well: FMD% 4.12+/-3.96% vs. 11.12+/-7.22% (p=0.007). No difference was found in FID% before and after 3 months of treatment: 20.97+/-10.66% vs.17.94+/-6.23% (p=NS). CONCLUSIONS: Periodontitis may be an insidious cause of endothelial dysfunction and cardiovascular events. Treating periodontitis can improve endothelial function and be an important preventive tool for cardiovascular disease.

Varicella zoster infection and pulmonary complications.

A 34-year-old immunocompetent man with varicella zoster (VZ) infection developed deep vein thrombosis and pulmonary embolism after suffering severe pneumonitis. He recovered after treatment with acyclovir, high-dose steroids, and ventilatory support. The endothelial damage could be a direct link between VZ pneumonitis and pulmonary emboli.

Endothelial function in patients with sickle cell anemia during and after sickle cell crises.

BACKGROUND: Prior studies have demonstrated increased adherence of sickle cell erythrocytes to vascular endothelial cells. While decreased production of nitric oxide and increased production of adhesion molecules have been implicated in this pathophysiology, the relative contribution of these mechanisms during acute sickle cell crises as compared to steady state conditions have not been elucidated. METHODS AND RESULTS: We studied 10 consecutive young adult patients presenting with a sickle cell crisis. Endothelial function was evaluated by a non-invasive brachial artery shear stress method. Serum levels of adhesion molecules were obtained during the crisis. Both brachial artery responsiveness and serum levels of adhesion molecules were then repeated at steady state. Ten age and gender matched volunteers served as a control group. Impaired endothelial function and impaired endothelium-independent vasodilatation were observed in all sickle cell patients during both steady state and during crisis. Flow mediated dilation (FMD)% was 3.25+/- 2.76% during crisis, 4.57+/- 4.11 at steady state, compared with the control group FMD of 11.64+/- 7.69% (p< 0.001). Flow independent dilation was 10.35+/- 11.3% during crisis, 10.03+/- 6.52% at steady state, compared with control group FID of 24.17+/- 11.87% (p< 0.001). Levels of cell adhesion molecules and markers of inflammation were increased in sickle cell crisis patients compared with the control group: sCD40 ligand levels during the acute crisis were over twice the level of normal matched volunteers (p=0.02), and similarly significant increases were seen for E-selectin (p=0.008), ICAM-1 (p=0.037) and VCAM-1 levels (p=0.01). The levels of each of these biomarkers was not significantly increased during acute crises as compared to patients' recovery state. CONCLUSIONS: Sickle cell anemia patients have severe systemic endothelial dysfunction as demonstrated by both brachial artery assessment and increased serum levels of adhesion molecules. These abnormalities characterize not only the sickle cell crisis but also the steady state pathophysiology of sickle cell anemia.