Sjögren's Syndrome with Chronic Pancreatitis, Sclerosing Cholangitis, and Pulmonary Infiltrations

We report a patient with Sjögren's syndrome and multiple gastrointestinal manifestations who successfully responded to therapy with ursodeoxycholic acid. Our patient had sialoadenitis with dry mouth, dry eyes, arthralgia, chronic pancreatitis, sclerosing cholangitis, and pulmonary inflitrations. The first signs of disease were the symptoms of chronic pancreatitis followed by icterus, caused by extrahepatic bile duct obstruction. Sclerosing cholangitis was diagnosed by liver biopsy and endoscopic retrograde cholangiography. Sialoadenitis, causing dry mouth, was verified by buccal biopsy. Pulmonary infiltrations were seen on standard chest x-ray, and also shown by high-resolution computed tomography examination. Obstructive icterus and even pulmonary infiltration responded successfully to treatment with ursodeoxycholic acid.     

Design, spectrum measurements and simulations for a 238Pu alpha-particle irradiator for bystander effect and genomic instability experiments.

Design, spectrum measurements and simulations for an alpha-particle irradiator for bystander effect and genomic instability experiments are presented. Measured alpha-particle energy spectra were used to confirm the characteristics of the source of the irradiator specified by the manufacturer of the source. The spectra were measured in vacuum with a high-resolution spectrometer and simulated with an AASI Monte Carlo code. As a next step, we simulated alpha-particle energy spectra at the target plane of the irradiator for three different source-to-target distances. In these simulations, helium was used as the medium between the source and the exit window of the irradiator; its pressure and temperature corresponded to those of the ambient air. Mean energies and full-widths at half-maximum (FWHM) were calculated for the three different helium gas tracks.     

Self-warming blanket versus forced-air warming blanket during total knee arthroplasty under spinal anaesthesia: A randomised non-inferiority trial

Background

Arthroplasty patients are at high risk of hypothermia. Pre-warming with forced air has been shown to reduce the incidence of intraoperative hypothermia. There is, however, a lack of evidence that pre-warming with a self-warming (SW) blanket can reduce the incidence of perioperative hypothermia. This study aims to evaluate the effectiveness of an SW blanket and a forced-air warming (FAW) blanket peri-operatively. We hypothesised that the SW blanket is inferior to the FAW blanket.

Methods

In total, 150 patients scheduled for primary unilateral total knee arthroplasty under spinal anaesthesia were randomised to this prospective study. Patients were pre-warmed with SW blanket (SW group) or upper-body FAW blanket (FAW group) set to 38°C for 30 min before spinal anaesthesia induction. Active warming was continued with the allocated blanket in the operating room. If core temperature fell below 36°C, all patients were warmed using the FAW blanket set to 43°C. Core and skin temperatures were measured continuously. The primary outcome was core temperature on admission to the recovery room.

Results

Both methods increased mean body temperature during pre-warming. However, intraoperative hypothermia occurred in 61% of patients in the SW group and in 49% in the FAW group. The FAW method set to 43°C could rewarm hypothermic patients. Core temperature did not differ between groups on admission to the recovery room, p = .366 (CI: −0.18–0.06).

Conclusions

Statistically, the SW blanket was non-inferior to the FAW method. Yet, hypothermia was more frequent in the SW group, requiring rescue warming as we strictly held to the NICE guideline.

Trial Registration

Clinicaltrials.gov identifier: NCT03408197.     

Mitochondrial genome mutations in hypertensive individuals

Human essential hypertension (HTN), a polygenic, multifactorial, and highly heterogeneous disorder of unknown etiology, has been shown to have excess maternal transmission in several studies, suggesting a possible mitochondrial involvement. In an effort to assess the contribution of the mitochondrial genome to HTN we initiated a systematic, extended screening of hypertensive individuals to identify potentially pathogenic mtDNA mutations. We applied our newly developed novel class of tests for the detection of mitochondrial mutation involvement in complex diseases to the hypertension data set from 350 pedigrees of white ethnicity and 98 of African American ethnicity ascertained at HTN clinics associated with Boston Medical Center, and we identified families with a likely mitochondrial involvement. We analyzed the sequence of the entire mitochondrial genome in probands from 20 such pedigrees, consisting of 10 African American and 10 white families. Comparison with the reference "Cambridge" sequence revealed a total of 297 base changes, including 24 in the ribosomal RNA (rRNA) genes, 15 in the transfer RNA (tRNA) genes, and 46 amino acid substitutions, with the remainder involving the noncoding regions or synonymous changes. Among the coding region mutations, 30 are novel, with 13 hypertensive probands carrying at least one novel variant, usually in combination with the previously described common polymorphisms, several of which are associated with cardiovascular and renal pathologies. These data will serve as a starting point for large-scale case-control association studies.     

Gastric air tonometry during laparoscopic cholecystectomy: a comparison of two PaCO2 levels

PURPOSE: Pneumoperitoneum can cause disturbances in acid-base balance and splanchnic perfusion. We studied the effect of ventilation on acid-base balance and gastric mucosal tonometric values in patients undergoing laparoscopic cholecystectomy. METHODS: Twenty-four patients (ASA I-II) were randomly allocated into two groups. In the fixed ventilation group, ventilation was constant allowing free increase in PCO2, while in the constant CO2 group end-tidal PCO2 was fixed with ventilatory adjustment. Intraabdominal pressure was limited to 12 mmHg. Arterial acid-base balance, automated air tonometric variables and gastric mucosal to arterial PCO2 gap were determined frequently from anesthesia induction until three hours postoperatively. RESULTS: During pneumoperitoneum, in the fixed ventilation group arterial PCO2 changed from 5.0 +/- 0.2 to 6.6 +/- 0.4 kPa and pH from 7.43 +/- 0.03 to 7.33 +/- 0.04, tonometric PCO2 from 5.1 +/- 0.5 to 6.9 +/- 0.4 and pH from 7.44 +/- 0.04 to 7.33 +/- 0.04. In the constant CO2 group these variables remained at control levels (P < 0.01 between groups). The PCO2 gap remained unchanged without any differences between the groups. In the recovery room all measured variables were within normal range in both groups. CONCLUSION: Despite inter-group differences in arterial and tonometric PCO2 and pH values during CO2 pneumoperitoneum, the patients did not develop splanchnic hypoperfusion detectable by air tonometric method, as indicated by normal PCO2 gap in both groups throughout the study.     

Epileptiform Electroencephalogram during Mask Induction of Anesthesia with Sevoflurane

Background: Sevoflurane is suggested as a suitable anesthetic agent for mask induction in adults. The authors recently found that hyperventilation during sevoflurane-nitrous oxide-oxygen mask induction is associated with cardiovascular hyperdynamic response. We tested the hypothesis that the hyperdynamic response can be explained by electroencephalography (EEG) findings.

Methods: Thirty women were randomly allocated to receive sevoflurane-nitrous oxygen-oxygen mask induction using a single-breath method, followed by either spontaneous breathing (n = 15) or controlled hyperventilation (n = 15) for 6 min. EEG was recorded. Blood pressure and heart rate were recorded at 1-min intervals.

Results: Epileptiform EEG activity (spikes or polyspikes) was seen in all patients with controlled hyperventilation, and in seven patients with spontaneous breathing (P< 0.01). Jerking movements were seen in three patients with controlled hyperventilation. In the controlled hyperventilation group, heart rate increased 54% from baseline at 4 min after induction (P< 0.001). Mean arterial pressure increased 17% (P< 0.05), peaking at 3 min. In the spontaneous breathing group, heart rate showed no change, and mean arterial pressure decreased by 14% (P< 0.01) at 6 min. Heart rate and mean arterial pressure differed significantly between the groups from 2 min after beginning of the induction to the end of the trial. An increase in heart rate of more than 30% from baseline always was associated with epileptiform EEG activity.     

Rotator cuff calcifications: treatment with ultrasound-guided percutaneous needle aspiration and lavage

 Objective. To analyze the results of ultrasound (US)-guided needle puncture, aspiration and lavage in the treatment of symptomatic calcific tendinitis of the rotator cuff. Design and patients. Atraumatic pain in 61 shoulders of 58 patients was resistant to conservative therapy. The average age of the treated patients was 42 years (range 26–49 years), follow-up was 12 months, and the mean diameter of the calcifications was 1.6 cm (range 1.1–2.9 cm). With US guidance and local anesthesia, two needles were placed within each calcification. The calcification was punctured 10–15 times and saline solution injected and aspirated using the needles until the aspirate was free of calcific particles. Results and conclusions. Based on radiographs at 1 year follow-up, 74% (45 of 61) of the calcifications decreased, including 28% (17 of 61) which disappeared totally, and 26% (16 of 61) were unchanged. Calcifications with a faint or absent shadow on US proved to be nearly liquid (slurry calcification in 93% (14 of 15) of cases and could be aspirated. Clinical results were excellent in 74% (45 of 61), moderate in 16% (10 of 61) and poor in 10% (6 of 61) of cases. US offers technical advantages over fluoroscopy, and the typical US image of a slurry calcification helps to select the most suitable patients for aspiration treatment. The results are comparable with those using fluoroscopic guidance.     

Inhibition of ACTH-induced differentiation of cortical cells and their mitochondria by corticosterone in tissue culture of fetal rat adrenals

Tissue cultures of fetal rat adrenals were used to study the effects of corticosterone on the ACTH-induced ultrastructural differentiation of cortical cells and their mitochondria. Corticosterone in dosages of 0.2, 2.0, 5.0, 10, and 20 μg/ml (corresponding to concentrations of 6 × 10^?7, 6 × 10^?6, 1.5 × 10^?5, 3 × 10^?5, and 6 × 10^?5 molar) was added alone or together with 100 mU/ml of ACTH to the culture medium, daily from the sixteenth day of cultivation up to and including the twenty-first day. Corticosterone alone induced no ultrastructural changes in cortical cells. Corticosterone in concentrations of 6 × 10^?7 to 3 × 10^?5 M given with ACTH induced hypertrophy of Golgi apparatus. Corticosterone in concentrations of 6 × 10^?5 M inhibited the ACTH-induced differentiation of cortical cells. However, the nuclear chromatin increased and Golgi apparatus was strikingly hypertrophied. Mitochondria often aggregated adjacent to the nuclear envelope but their ultrastructure remained undifferentiated with tubular or tubulovesicular cristae. Ribosomes appeared as single particles. A marked increase of smooth surfaced endoplasmic reticulum was noted also in cortical cells treated with 6 × 10^?5 M of corticosterone. The present observations suggest that corticosterone acts as an intracellular inhibitor in cortical cells. It appears to inhibit cytoplasmic protein synthesis at the ribosomal level and prevents synthesis of cytoplasmic mitochondrial protein synthesis stimulating factor and the latter, in turn, inhibits the activation of mitochondrial protein synthesis. A new model is presented to explain the regulation of growth and secretion in the adrenal cortex.     

Angiotensin-converting enzyme inhibition after experimental myocardial infarct: role of the kinin B1 and B2 receptors

We sought to define the contribution of each of the 2 kinin receptors (bradykinin 1 receptor [B(1)R] and bradykinin 2 receptor [B(2)R]) to the cardioprotection of angiotensin-converting enzyme (ACE) inhibition after acute myocardial infarct. Wild-type mice and gene knockout mice missing either B(1)R or B(2)R were submitted to coronary ligation with or without concurrent ACE inhibition and had evaluation of left ventricular systolic capacity by assessment of fractional shortening (FS). Baseline FS was similar in all of the animals and remained unchanged in sham-operated ones. At 3 weeks after myocardial infarct, in the wild-type group there was a 27% reduction of FS (P<0.5) without ACE inhibition and 8% with ACE inhibition; in the B(1)R(-/-) groups the FS was reduced by 24% and was no different (at 28%) with ACE inhibition; in the B(2)R(-/-) groups, however, the FS was decreased by 39% and with ACE inhibition was decreased further by 52%. Analysis of bradykinin receptor gene expression in hearts showed that when one receptor was missing, the other became significantly upregulated; but the B(1)R remained highly overexpressed in the B(2)R(-/-) mice throughout, whereas the overexpressed B(2)R became significantly suppressed in the B(1)R(-/-) mice in a manner quantitatively and directionally similar to that of wild-type mice. We conclude that both bradykinin receptors contribute to the cardioprotective bradykinin-mediated effect of ACE inhibition, not only the B(2)R as believed previously; but, whereas with potentiated bradykinin in the absence of B(1)R, the upregulation of B(2)R is simply insufficient to provide full cardioprotection, in the absence of B(2)R, the upregulated B(1)R actually seems to inflict further tissue damage.     

Endorsement of clinical practice guidelines by the Scandinavian Society of Anaesthesiology and Intensive Care Medicine

Clinical practice guidelines from other organizations or societies with assumed clinical and contextualized relevance for Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI) members, may trigger a formal evaluation by The Clinical Practice Committee (CPC) for possible SSAI endorsement. This avoids unnecessary duplicate processes and minimizes resource-waste. Identified guidelines are assessed for endorsement using the Appraisal of Guidelines for REsearch and Evaluation (AGREE) II instrument. The SSAI CPC utilizes the AGREE II online coordinated group appraisal platform to assess the methodological rigor and transparency in which the guideline was developed. The results of the assessment, including the decision to endorse or not, are presented to the SSAI Board for sanctioning. This document briefly outlines the process for evaluation of non-SSAI guidelines by the CPC for possible SSAI endorsement.