Lung ultrasound B-lines are correlated with lung weight and density determined by CT. LUS may provide a reliable, simple and radiation-free lung densitometry in the intensive care setting.

Malunion after a distal radius fracture can be treated with an osteotomy of the distal radius. Autologous iliac crest bone graft is often used to fill the gap, but the procedure is associated with donor site morbidity. In this study a novel fast resorbing biphasic bone substitute consisting of a mixture of calcium sulphate and calcium phosphate is used (Cerament BoneSupport AB, Sweden). Fifteen consecutive patients, with a mean age of 52 (27-71) years were included. All had a malunion after a distal radius fracture and underwent an osteotomy. A fragment specific fixation system, TriMed (TriMed, Valencia, CA), consisting of a Buttress Pin and a Radial Pin Plate were used for fixation and a calcium sulphate and calcium phosphate mixture as bone substitute. The patients were followed for 1 year. Grip strength increased from 61 (28-93)% of the contralateral hand to 85 (58-109)%, p < 0.001. DASH scores decreased from 37 (22-61) to 24 (2-49) p = 0.003. Radiographically all osteotomies healed. An increase of ulnar variance was noted during healing from 1.8 mm immediately postoperatively to 2.6 mm at final follow up. Osteotomy can increase grip strength and decease disability after a malunited fracture. In the present series the bone substitute was replaced by bone, but a minor loss of the achieved radiographic correction was noted in some patients during osteotomy healing. A more rigid fixation may improve the radiographic outcome with this kind of bone substitute.

Background and purpose In unstable distal radial fractures that are impossible to reduce or to maintain in reduced position, the treatment of choice is operation. The type of operation and the choice of implant, however, is a matter of discussion. Our aim was to investigate whether open reduction and internal fixation would produce a better result than traditional external fixation.Methods 50 patients with an unstable or comminute distal radius fracture were randomized to either closed reduction and bridging external fixation, or open reduction and internal fixation using the TriMed system. The primary outcome parameter was grip strength, but the patients were followed for 1 year with objective clinical assessment, subjective outcome using DASH, and radiographic examination.Results At 1 year postoperatively, grip strength was 90% (SD 16) of the uninjured side in the internal fixation group and 78% (17) in the external fixation group. Pronation/supination was 150° (15) in the internal fixation group and 136° (20) in the external fixation group at 1 year. There were no differences in DASH scores or in radiographic parameters. 5 patients in the external fixation group were reoperated due to malunion, as compared to 1 in the internal fixation group. 7 other cases were classified as radiographic malunion: 5 in the external fixation group and 2 in the internal fixation group.Interpretation Internal fixation gave better grip strength and a better range of motion at 1 year, and tended to have less malunions than external fixation. No difference could be found regarding subjective outcome.

Fracture dislocations of the PIP joint are challenging to treat. In hemi-hamate arthroplasty, the palmar lip joint surface is reconstructed using an osteochondral graft from the hamate and the immediate stability permits early movement. In the long term, collapse of non-vascularized osteochondral grafts might lead to degenerative arthritis. We examined the radiographic result after a minimum of 4 years with special reference to the development of osteoarthritis and its relation to clinical symptoms in eight patients, mean age 49 (25-66) years. After a mean of 60 (48-69) months, the arc of motion was 67° (45°-95°) at the PIP joint and grip strength was 91% of the uninjured side. The visual analogue score for pain (0-100) was 10 (0-70) mm. Severe arthritis (grade IV) was found in two and mild arthritis (grade II) in another two patients, but only one of these four cases had troublesome pain. The hemi-hamate technique is an attractive alternative to other treatment options, but some cases develop osteoarthritis in the medium term.

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) can be associated with severe adverse digestive effects. In clinical settings, proton pump inhibitors have proven to be effective in preventing and healing NSAID-induced gastroduodenal lesions. The present study investigates the mechanisms of protection afforded by pantoprazole against gastric injury induced by different NSAIDs in rats. Animals were orally treated with indomethacin (100 micromol/kg), diclofenac (60 micromol/kg), piroxicam (150 micromol/kg) or ketoprofen (150 micromol/kg). Thirty minutes before NSAIDs, animals received pantoprazole 6 or 60 micromol/kg orally. Four hours after NSAIDs, the following parameters were assessed: histomorphometric evaluation of gastric mucosal damage; gastric mucosal levels of myeloperoxidase (MPO), malondialdehyde (MDA), reduced glutathione as an index of non-proteic sulfhydryl compounds (GSH), and prostaglandin E2 (PGE2); mucosal cyclooxygenase-1 and -2 (COX-1, COX-2) mRNA expression by reverse transcription-polymerase chain reaction (RT-PCR). Separate experiments were carried out to assay the effects of pantoprazole on gastric acid secretion in pylorus-ligated rats. The in vitro influence of pantoprazole (1-10 microM) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate was also examined. All NSAIDs elicited mucosal necrotic lesions associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels, were detected in the gastric mucosa of indomethacin-, piroxicam- or ketoprofen-treated animals. Indomethacin enhanced mucosal COX-2 expression, while not affecting COX-1. At the oral dose of 6 micromol/kg pantoprazole did not affect NSAID-induced mucosal damage, whereas at 60 micromol/kg it markedly reduced injuries provoked by all test NSAIDs. Pantoprazole 60 micromol/kg also reversed the effects of NSAIDs on MPO, MDA, and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced COX-2 expression. However, at both doses, pantoprazole inhibited acid secretion in pylorus-ligated rats. Furthermore, pantoprazole concentration dependently reduced the in vitro oxidation of LDLs. Our results suggest that besides inhibiting acid secretion, the protection afforded by pantoprazole against NSAID-induced gastric damage depends on a reduction in mucosal oxidative injury, which may also account for an increment of sulfhydryl radical mucosal bioavailability. It is also suggested that pantoprazole does not influence the down-regulation of gastric prostaglandin production associated with NSAID treatment.