The quadruple cruciate sign of simultaneous bicompartmental medial and lateral bucket-handle meniscal tears.

We report the second known case of bicompartmental bucket-handle tears of the medial and lateral menisci and the first documented case of the bucket-handle tears occurring simultaneously following trauma, which occurred after a motorcycle accident. Both bucket-handle fragments were displaced into the intercondylar notch. An anterior cruciate ligament tear was also present. Coronal images demonstrated four structures in the intercondylar notch: the anterior and posterior cruciate ligaments and the medial and lateral bucket-handle meniscal fragments.

Implications of early sonographic evaluation of parapneumonic effusions in children with pneumonia.

OBJECTIVE: To devise a clinically relevant grading system for the sonographic evaluation of parapneumonic effusions, and to evaluate length of hospital stay as a function of treatment approach and sonographic grades. METHODS: Chest sonograms of 46 pediatric patients diagnosed with empyemas and admitted to two medical centers in the last 8 years were retrospectively evaluated using a grading system based on the degree of fibrinous organization within the parapneumonic effusions. Hospital charts were reviewed to determine the method of treatment and length of hospital stay. Patients were divided into two treatment groups: nonoperative (n = 26) (antibiotics alone, or combined with thoracentesis, or tube thoracostomy) and operative (n = 20) (open decortication, or video thoracoscopy and pleural debridement). Patients in the nonoperative group were further subdivided into two groups: those who received antibiotics alone (n = 11) and those who received antibiotics plus nonoperative drainage thoracentesis and/or tube thoracostomy (n = 15). Within each treatment group, patients were subdivided into two ultrasound grades: low (no evidence of organization) and high (evidence of organization such as fronds, septations, or loculations). Student's t test was performed to compare the lengths of hospital stay for each of the treatment groups and ultrasound grades. RESULTS: The length of hospitalization was no different for patients with low-grade ultrasounds in the nonoperative (9.8 days) and operative groups (8.0 days). In contrast, length of hospitalization was significantly shorter for patients with high-grade sonograms in the operative group (8.6 days), when compared with the nonoperative group (16.4 days). Length of hospitalization for patients in the nonoperative group with high-grade sonograms was significantly longer (16.4 days) than for those with low-grade ultrasounds (9.8 days). Furthermore, when the nonoperative patients were divided into an antibiotics alone group and a nonoperative drainage group, the patients with low-grade sonograms had no difference in the length of hospitalization (9.0 days vs. 10.4 days), whereas those patients with high-grade sonograms in the nonoperative drainage group had a significantly longer hospitalization (19.9 days) than the antibiotics alone (high-grade) group (11.4 days). CONCLUSIONS: Patients with a low-grade sonogram had similar length of hospitalization if treated with either nonoperative or operative measures. Patients with high-grade sonograms had significantly shorter length of hospitalization when treated with decortication. Our retrospective study suggests that patients with high-grade ultrasound studies treated nonoperatively do not benefit from pleural drainage procedures or chest tube placement. This study demonstrates the usefulness of early sonographic evaluation of parapneumonic effusions. A prospective study evaluating the usefulness of sonographic assessment of severity of disease in the treatment of children with parapneumonic effusions is warranted on the basis of our retrospective data.

Neuronal injury evoked by depolarizing agents in rat cortical cultures.

Chemical depolarization is often used to study neurotransmitter release. Three commonly used depolarizing agents, veratridine, potassium, and glutamate, were evaluated for neurotoxicity. Neuronal survival and lactate dehydrogenase efflux were measured to assay irreversible injury. In addition, video-enhanced differential interference contrast microscopy was used to measure acute neuronal swelling. We found that lactate dehydrogenase efflux and cell death associated with exposure to potassium and glutamate could be blocked by the competitive N-methyl-D-aspartate antagonist amino-phosphonovaleric acid. Neuronal swelling was observed with all three agents, and could not be blocked by amino-phosphonovaleric acid. These results suggest multiple mechanisms of neuronal injury accompanying chemical depolarization. A 60-min exposure to 100 microM veratridine increased lactate dehydrogenase appearing in the medium at the end of this exposure to 615% of control and produced a 62% loss of neurons after 20-24 h. These effects could not be blocked by amino-phosphonovaleric acid at 500 microM. Differential interference contrast imaging revealed acute neuronal swelling in response to veratridine within 5 min of exposure, and this swelling could not be blocked by amino-phosphonovaleric acid. A 60-min exposure to medium supplemented with 50 mM KCl caused a lactate dehydrogenase efflux of 204% of control and produced a 48% loss of neurons. Amino-phosphonovaleric acid blocked both the neuronal loss and the excess lactate dehydrogenase efflux. In addition, differential interference contrast monitoring showed no KCl-evoked swelling. In contrast, isotonic substitution of 50 mM KCl for NaCl resulted in acute swelling which could not be blocked by amino-phosphonovaleric acid, in addition to neuronal death and lactate dehydrogenase release. Glutamate was, as expected, neurotoxic, and as has been shown before, this toxicity could be blocked by amino-phosphonovaleric acid. Observation of neurons exposed to 300 microM glutamate revealed that this treatment was invariably associated with neuronal swelling. In the presence of amino-phosphonovaleric acid, 81% of neurons swelled to greater than 110% by 30 min exposure to glutamate. These results suggest that experimental paradigms which investigate the effects of chemical depolarization upon central neurons are likely to be associated with reversible and irreversible forms of injury. This is of special importance to any study of the mechanisms of release of substances from central neurons.