Percutaneous cholecystostomy is an effective definitive treatment option for acute acalculous cholecystitis.

AIMS: Acute acalculous cholecystitis can be treated with percutaneous cholecystostomy in critically ill patients unfit for surgery. However, the evidence on the outcome is sparse. We conducted a retrospective analysis of acute acalculous cholecystitis patients treated with percutaneous cholecystostomy during a 10-year study period. METHODS: An observational study of 56 consecutive patients treated with percutaneous cholecystostomy for acute acalculous cholecystitis was conducted in the period from 1 June 2002 to 31 May 2012. All data were obtained by review of medical records. RESULTS: A total of 56 consecutive patients were treated with percutaneous cholecystostomy for acute acalculous cholecystitis. Six patients (10.7%) died within 30 days after the procedure. Percutaneous cholecystostomy could serve as a definitive treatment option in 45 patients (80.4%), whereas 1 patient (1.8%) required cholecystectomy due to recurrence of cholecystitis. Four patients (7.1%) were treated with percutaneous cholecystostomy as a bridging procedure to subsequent elective laparoscopic cholecystectomy within a median of 8.8 months (range: 7.7-33.4 months). There was no significant difference in the risk of cholecystitis recurrence between patients with (6/37) and without (2/3) contrast passage to the duodenum on cholangiography (p = 0.096). CONCLUSION: Percutaneous cholecystostomy is successful as a definitive treatment option in the majority of patients with acute acalculous cholecystitis. It is associated with a low rate of mortality and subsequent cholecystectomy.

Heart rate limitation and cardiac unloading in sevoflurane post-conditioning.

BACKGROUND: Sevoflurane post-conditioning (SePost) has been found to alleviate ischemic myocardial reperfusion injury through the activation of prosurvival kinases. Lowered myocardial oxygen demand from reduced cardiac work may also contribute to cardioprotection, and is much less well-studied. Our aim was to examine the simultaneous effects of SePost on cardiac work (here, rate-pressure product, RPP) and myocardial infarct size in a porcine model. METHODS: Anesthetized 25 kg pigs were randomly allocated to two groups and underwent 45 min regional coronary artery balloon occlusion and subsequent 2 h reperfusion. SePost (n = 10) was given as sevoflurane 1.5-3% end-tidal concentration during reperfusion while controls (n = 12) were untreated. Aortic blood pressure was measured directly, while mixed-venous oxygen saturation and cardiac output were measured in the pulmonary artery. Cardiac work was determined as RPP. Post-mortem, histologic myocardial infarct size (IS), and area at risk were determined in transverse heart slices after tetrazolium stain. RESULTS: Myocardial infarct size was reduced from (control) 55.0 (mean) ± 13.6% (standard deviation) to 32.5 ± 13.4% in group SePost (P = 0.0009). During reperfusion, SePost resulted in lower heart rate (P = 0.0003), cardiac output (P = 0.0123), mixed-venous oxygen saturation (P = 0.0103), blood pressure, and RPP (P < 0.0001). RPP was highly correlated to IS (P = 0.0055). CONCLUSION: SePost (1.5-3%) reduced infarct size after regional myocardial ischemia in vivo and reduced cardiac work was significantly correlated to myocardial salvage.

Hypertrophied hearts: what of sevoflurane cardioprotection?

BACKGROUND: Recent studies have demonstrated that inhalation anaesthetics, like sevoflurane, confer cardioprotection both experimentally and clinically. However, coexisting cardiac disease might diminish anaesthetic cardioprotection and could partly explain why the clinical results of cardioprotection with anaesthetics remain controversial--in contrast to solid experimental evidence. Concomitant left ventricular hypertrophy is found in some cardiac surgery patients and could change cardioprotection efficacy. Hypertrophy could potentially render the heart less susceptible to sevoflurane cardioprotection and more susceptible to ischaemic injury. We investigated whether hypertrophy blocks sevoflurane cardioprotection, and whether tolerance to ischaemia is altered by left ventricular hypertrophy, in an established experimental animal model of ischaemia-reperfusion. METHODS: Anaesthetized juvenile pigs (n=7-12/group) were subjected to 45 min distal coronary artery balloon occlusion, followed by 120 min of reperfusion. Controls were given pentobarbital, while sevoflurane cardioprotection was achieved by 3.2% inhalation throughout the experiment. Chronic banding of the ascending aorta resulted in left ventricular hypertrophy development in two further groups and these animals underwent identical ischaemia-reperfusion protocols, with or without sevoflurane cardioprotection. Myocardial infarct sizes were compared post-mortem. RESULTS: The mean myocardial infarct size (% of area-at-risk) was reduced from mean 55.0 (13.6%) (+/-SD) in controls to 17.5 (13.2%) by sevoflurane (P=0.001). Sevoflurane reduced the infarct size in hypertrophied hearts to 14.6 (10.4%) (P=0.001); however, in hypertrophic controls, infarcts were reduced to 34.2 (10.2%) (P=0.001). CONCLUSION: Sevoflurane abrogated ischaemic injury to similar levels in both normal and left ventricular hypertrophied hearts.

Quality of plasma sampled by different methods for multiple blood sampling in mice.

For oral glucose tolerance test (OGTT) in mice, multiple blood samples need to be taken within a few hours from conscious mice. Today, a number of essential parameters may be analysed on very small amounts of plasma, thus reducing the number of animals to be used. It is, however, crucial to obtain high-quality plasma or serum in order to avoid increased data variation and thereby increased group sizes. The aim of this study was to find the most valid and reproducible method for withdrawal of blood samples when performing OGTT. Four methods, i.e. amputation of the tail tip, lateral tail incision, puncture of the tail tip and periorbital puncture, were selected for testing at 21 degrees C and 30 degrees C after a pilot study. For each method, four blood samples were drawn from C57BL/6 mice at 30 min intervals. The presence of clots was registered, haemolysis was monitored spectrophotometrically at 430 nm, and it was noted whether it was possible to achieve 30-50 microL blood. Furthermore, a small amount of extra blood was sampled before and after the four samplings for testing of whether the sampling induced a blood glucose change over the 90 min test period. All methods resulted in acceptable amounts of plasma. Clots were observed in a sparse number of samples with no significant differences between the methods. Periorbital puncture did not lead to any haemolysed samples at all, and lateral tail incision resulted in only a few haemolysed samples, while puncture or amputation of the tail tip induced haemolysis in a significant number of samples. All methods, except for puncture of the tail tip, influenced blood glucose. Periorbital puncture resulted in a dramatic increase in blood glucose of up to 3.5 mmol/L indicating that it is stressful. Although lateral tail incision also had some impact on blood glucose, it seems to be the method of choice for OGTT, as it is likely to produce a clot-free non-haemolysed sample, while periorbital sampling, although producing a high quality of sample, induces such a dramatic change in blood glucose that it should not be applied for OGTT in mice.

Radioimmunotherapy of acquired immunodeficiency syndrome (AIDS) associated lymphoma.

Standard therapy for AIDS associated NHL (AANHL) is toxic and often ineffective. Radioimmunotherapy (RIT) is an appealing alternative to chemotherapy because of the radiosensitivity of NHL and the ability of the Lym-1 monoclonal antibody to target therapeutic irradiation to NHL while relatively sparing normal tissue. A Phase I/II study of 90Y-2IT-BAD-Lym-1 was designed specifically for RIT of AANHL. The first patient has been treated with 15 mCi (7.5 mCi/m2) of 90Y-2IT-BAD-Lym-1, after an imaging dose of 111In-2IT-BAD-Lym-1. Before RIT, AANHL in the maxillary sinus extended into the oral cavity and axillary adenopathy was present. Imaging showed excellent accumulation of 111In-2IT-BAD-Lym-1 in the tumors. Substantial shrinkage of the oral lymphoma was observed 18 hours after the therapy dose of 90Y-2IT-BAD-Lym-1 and axillary adenopathy had disappeared by one week after RIT. Transient Grade IV myelosuppression was the only notable toxicity. Further RIT cycles were precluded by development of an antibody response (HAMA) against Lym-1. This novel preliminary study has shown that Lym-1 can target AANHL and produce significant tumor regression thereby providing encouragement to proceed with additional patients.