State of the art in factor XIII laboratory assessment.

Factor XIII, a heterotetrameric proenzyme, is converted to an activated transglutaminase by thrombin and calcium in the final phases of coagulation. Factor XIII catalyzes the formation of crosslinks between fibrin monomers and between α2-antiplasmin and fibrin. These crosslinks mechanically stabilize fibrin against shear stress, enable red cell retention within the clot, and protect the clot from premature degradation. Congenital factor XIII deficiency is caused by autosomal recessive mutations, presenting early in life with a severe bleeding diathesis. Acquired deficiency may be caused by autoimmunity. Currently available assays for laboratory diagnosis of factor XIII deficiency include clot solubility assays, quantitative factor XIII activity assays, factor XIII antigen assays, and genetic testing. The International Society on Thrombosis and Haemostasis Scientific and Standardization Committee has recommended an algorithm for the laboratory diagnosis and differentiation of the different forms of factor XIII deficiency. However, implementation of this algorithm has been limited by technical and budgetary challenges associated with the currently available factor XIII-specific assays. The purpose of this review is to discuss the advantages and limitations of the currently available assays employed for the laboratory diagnosis of factor XIII deficiency.

Physiologically Triggered Digital Cognitive Aid Facilitates Crisis Management in a Simulated Operating Room: A Randomized Controlled Study.

INTRODUCTION: Although the benefits of using cognitive aids in anesthesia care have previously been demonstrated, several challenges remain. It must be presented in a timely manner, and providers must be amenable to using the tool once it is available. We hypothesized that anesthesia residents would perform superiorly when presented with a digital cognitive aid (DCogA) that is automatically triggered by a set vital sign aberration. METHODS: Thirty anesthesia residents were randomized to either control (with access to hard copy of the cognitive aid) or receive a DCogA projected on their anesthesia information management system with the onset of heart block and associated hypotension. The scenario ended upon commencement of pacing, and the times to interventions were recorded. RESULTS: Fourteen participants were randomized to the control group and 16 to the intervention group DCogA. In the control group, 6 of 14 participants failed to pace, and in the DCogA group, all participants initiated pacing (P < 0.01). Those in the DCogA group were also faster to pace [260.1 (137.5) s vs. 405.1 (201.8) s, P = 0.03]. Both groups were similar with respect to their knowledge of advanced cardiovascular life support as measured by a pretest (P = 0.92). CONCLUSIONS: We found those participants who were presented with electronic, physiologically triggered cognitive aids were more likely to appropriately treat heart block by initiating transcutaneous pacing. We believe that adoption of a high-functioning anesthesia information management system designed to detect physiologic perturbations and present appropriate decision support tools would lead to safer intraoperative care.

The Impact of Bariatric Surgery on Type 2 Diabetes Mellitus and the Management of Hypoglycemic Events.

Recent studies discussed the benefit of bariatric surgery on obese patients diagnosed with type 2 diabetes mellitus (T2DM). Several factors play an essential role in predicting the impact of bariatric surgery on T2DM, such as ABCD score (age, BMI, C-peptide, and duration of the disease), HbA1c, and fasting blood glucose, incretins [glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide (GIP)]. DiaRem score known to include factors such as age, HbA1c, medication, and insulin usage used to predict the remission of T2DM, but it has some limitations. An extensive literature search was conducted on PubMed and Google Scholar using keywords such as gastric bypass, T2DM, bariatric surgery, GLP-1, GIP, and post bariatric hypoglycemia. Restrictive-malabsorptive procedures are most effective in treating T2DM patients based on changes induced in appetite through regulation of gastrointestinal hormones, with decreased hunger and increased satiation. We provide a review of bariatric surgery influence on T2DM and management of post-intervention hypoglycemic events. Post-bariatric surgery hypoglycemia is a serious complication especially when patients develop life-threatening neuroglycopenia with loss of consciousness and seizure. The avoidance of this adverse event may be achieved by strict dietary modification including a restriction on carbohydrates as well as foods with high glycemic index. Further research will provide more information on post-bariatric surgery hyperinsulinemic hypoglycemia pathophysiology and management.

Mitral Valve Stenosis after Open Repair Surgery for Non-rheumatic Mitral Valve Regurgitation: A Review.

Mitral stenosis (MS) after mitral valve (MV) repair is a slowly progressive condition, usually detected many years after the index MV surgery. It is defined as a mean transmitral pressure gradient (TMPG) >5 mmHg or a mitral valve area (MVA) <1.5 cm(2). Pannus formation around the mitral annulus or extending to the mitral leaflets is suggested as the main mechanism for developing delayed MS after MV repair. On the other hand, early stenosis is thought to be a direct result of an undersized annuloplasty ring. Furthermore, in MS following ischemic mitral regurgitation (MR) repair, subvalvular tethering is the hypothesized pathophysiology. MS after MV repair has an incidence of 9-54%. Several factors have been associated with a higher risk for developing MS after MV repair, including the use of flexible Duran annuloplasty rings versus rigid Carpentier-Edwards rings, complete annuloplasty rings versus partial bands, small versus large anterior leaflet opening angle, and anterior leaflet tip opening length. Intraoperative echocardiography can measure the anterior leaflet opening angle, the anterior leaflet tip opening dimension, the MVA and the mean TMPG, and may help identify patients at risk for developing MS after MV repair.

Opioid-induced hyperalgesia in chronic pain patients and the mitigating effects of gabapentin.

Chronic pain patients receiving opioid drugs are at risk for opioid-induced hyperalgesia (OIH), wherein opioid pain medication leads to a paradoxical pain state. OIH involves central sensitization of primary and secondary afferent neurons in the dorsal horn and dorsal root ganglion, similar to neuropathic pain. Gabapentin, a gamma-aminobutyric acid (GABA) analog anticonvulsant used to treat neuropathic pain, has been shown in animal models to reduce fentanyl hyperalgesia without compromising analgesic effect. Chronic pain patients have also exhibited lower opioid consumption and improved pain response when given gabapentin. However, few human studies investigating gabapentin use in OIH have been performed in recent years. In this review, we discuss the potential mechanisms that underlie OIH and provide a critical overview of interventional therapeutic strategies, especially the clinically-successful drug gabapentin, which may reduce OIH.