Is sarcopenia a useful predictor of outcome in patients after emergency laparotomy? A study using the NELA database.

Introduction Studies have reported on the use of frailty as a prognostic indicator in patients undergoing elective surgery. Similar data do not exist for patients undergoing emergency surgery. The aim of this study was to evaluate the effect of preoperative sarcopenia measured by computed tomography (CT) on outcome following emergency laparotomy. Materials and methods Data from the National Emergency Laparotomy Audit database were retrieved for patients who had undergone an emergency laparotomy over 12 months at York NHS Foundation Trust. Sarcopenia was assessed by psoas density and area on preoperative CT. Mortality rates at 30 days and 1 year were recorded. Secondary outcomes included discharge rates to non-independent living. Results A total of 259 patients were included. Overall cohort 30-day and 1-year mortality was 13.9% (36/259) and 28.2% (73/259), respectively. Sarcopenia measured by psoas density was associated with increased mortality compared with patients who did not develop sarcopenia at 30 days (29.7%, 19/64, vs. 8.7%, 17/195; P < 0.001; odds ratio, OR, 4.42; 95% confidence interval, CI 2.13-9.26) and at 1 year (57.8%, 37/64, vs. 18.5%, (36/195; P < 0.001; OR 6.05; 95%CI 3.28-11.18). An increase in mortality was seen in patients with sarcopenia measured by psoas area at 30 days (21.3%, 13/61, vs. 9.1%, 17/187; OR 2.71; 95%CI 1.23-5.96, P = 0.013) and at 1 year (42.6%, 26/61, vs. 20.9%, 39/187; OR 2.82; 95% CI 1.52-5.23, P < 0.001). Conclusions Sarcopenia assessed by measurement of psoas density and area on CT is associated with increased mortality following emergency laparotomy. The use of sarcopenia as a predictive tool merits further attention and may be useful in patients undergoing emergency surgery.

Purification, characterization and cloning of tensilin, the collagen-fibril binding and tissue-stiffening factor from Cucumaria frondosa dermis.

The inner dermis of the sea cucumber, Cucumaria frondosa, is a mutable collagenous tissue characterized by rapid and reversible changes in its mechanical properties regulated by one or more protein effectors that are released from neurosecretory cells. One such effector, tensilin, is a collagen-fibril binding protein, named for its ability to induce dermis stiffening. Tensilin was purified using an affinity column constructed from C. frondosa collagen-fibrils. The protein migrates as a single band on SDS-PAGE (Mr approximately 33 kDa) and has an isoelectric point of 5.8. Equilibrium sedimentation experiments suggest a molecular mass of approximately 28.5-29.4 kDa. Carbohydrate analysis of tensilin revealed no measurable sugar content. The molar amount of tensilin was determined to be 0.38% that of collagen and 47% that of stiparin, a constitutive matrix glycoprotein. A full-length cDNA clone for tensilin was obtained from a C. frondosa inner dermis cDNA expression library. Predicted properties derived from the deduced peptide sequence were in agreement with those of the native protein. A noted feature of tensilin's deduced peptide sequence, particularly in its N-terminal domain, is its homology to tissue inhibitor of metalloproteinases. Tensilin's C-terminal tail has no known homology to other proteins but contains a putative collagen-fibril binding site.

Functional morphology of the supraspinatus tendon.

Grossly normal supraspinatus tendons were analyzed by stereomicroscope dissection and three-dimensional serial-section reconstruction. Four structurally independent subunits were identified: the tendon proper extended from the musculotendinous junction to approximately 2.0 cm medial to the greater tuberosity. It was composed of parallel collagen fascicles oriented along the tensional axis and separated by a prominent endotenon region. There was no interdigitation of fascicles, and an 18% incidence of fascicle convergence as the fascicles coursed from muscle toward greater tuberosity. The attachment fibrocartilage extended from the tendon proper to the greater tuberosity, consisted of a complex basket-weave of collagen fibers, and stained diffusely with alcian blue. The densely packed unidirectional collagen fibers of the rotator cable extended from the coracohumeral (CH) ligament posteriorly to the infraspinatus, coursing both superficial and deep to the tendon proper. The capsule was composed of thin collagen sheets each with uniform fiber alignment that differed slightly between sheets. These data describe a specialized tendon capable of internally compensating for changing joint angles through fascicles which are structurally independent and can slide past one another. The tendon attachment exhibits a structure adapted to tensional load dispersion and resistance to compression.

Austrian triad with sinus of Valsalva aneurysm and rupture.

An interesting case of a young patient presenting with Austrian's Triad: pneumococcal pneumonia, pneumococcal meningitis, and pneumococcal endocarditis. On echocardiogram the patient was noted to have a noncoronary sinus of Valsalva aneurysm and vegetations on the aortic cusps resulting in disruption of valvular integrity and severe aortic insufficiency. Color Doppler also revealed rupture of the aneurysm into the right atrium. The patient was taken to surgery where the noncoronary cusp was noted to be completely replaced with vegetative lesions. The aortic valve was replaced with a No. 21 Carpentier-Edwards bioprosthetic valve (Edwards Lifesciences, Irvine, CA), and the noncoronary sinus of Valsalva was repaired with concomitant closure of the fistula using glutaraldehyde autologous pericardium.

New onset heart failure in a 29-year-old: A case report of isolated left ventricular noncompaction.

A previously healthy 29-year-old patient presented with new onset congestive heart failure. Based on findings on transthoracic echocardiogram (TTE) and cardiac magnetic resonance imaging (MRI) at an outside center, the patient was diagnosed as having a dilated cardiomyopathy with structural abnormalities in the ventricular septum and left ventricular (LV) apex suspicious for myocardial tumor. After referral to our center for further management, repeat TTE revealed findings characteristic of left ventricular non-compaction (LVNC) with severely depressed overall LV systolic function. Review of the outside cardiac MRI supported the diagnosis of LVNC. Final management consisted of traditional medical therapy for congestive heart failure, an implantable cardiac defibrillator (ICD), warfarin anticoagulation for the prevention of thromboembolism and referral for cardiac transplant.

Structure-function considerations of muscle-tendon junctions.

Skeletal muscle cells transmit force across the cell membrane to the extracellular matrix and ultimately to tendons. Force transmission may occur both along the lateral surfaces of muscle fibers and at their ends. Forces within muscles may follow the path of greatest resistance. Sites of force transmission are morphologically and compositionally specialized for this function. They are also specialized to provide stress-information that feeds into the synthetic programs of the muscle cell. A detailed analysis of the structures and functions of muscle-tendon junctions is essential to a comprehensive understanding of the way in which muscles and their connective tissues are controlled to move joints and to respond to mechanical stresses.

Identification of the encephalitogenic epitopes of CNS proteolipid protein in BALB/c mice.

It was previously shown that BALB/c mice were susceptible to experimental autoimmune encephalomyelitis induced by immunization with proteolipid protein (PLP). To determine the encephalitogenic epitopes of PLP in BALB/c mice, mice were immunized with successively smaller pools of 20-mer peptides spanning the PLP molecule from amino acid 30 to amino acid 206. Immunization with PLP(180-199) resulted in clinical EAE in 9/15 mice (mean max clinical score of 3.3), and immunization with PLP(185-206) induced clinical EAE in 7/21 BALB/c mice (mean maximum score of 3.7). No relapses in disease were observed. No EAE was observed in BALB/c mice immunized with PLP(185-199) (n=15), PLP(178-191) (n=13) or other regions of PLP (n=15). Passive transfer of PLP(180-199)-primed lymph node cells into nai;ve BALB/c mice resulted in EAE (2/2 mice, max score of 4.0). One-micron toluidine blue stained sections from the spinal cord of EAE-affected BALB/c mice revealed features typical of EAE in other strains, including mononuclear cell infiltration, myelin loss, and axonal loss.