Background: A standard approach to the recognition and management of major bleeding in immune thrombocytopenia (ITP) is lacking.Methods: Retrospective cohort study of ITP patients presenting to the emergency department (ED) with severe thrombocytopenia (platelet count <20 × 10 9 /L) and bleeding in four academic hospitals from 2008 to 2016. We defined a major ITP bleed as a bleed at a critical site or causing hemodynamic instability. Results:We identified 112 ITP patients (n = 141 visits) who presented to the ED with platelets <20 × 10 9 /L and bleeding. Twenty-nine patients (26%) had 32 ED visits with major bleeds. Risk factors for major bleeds were older age (odds ratio [OR] 1.03, 95% confidence interval [CI] 1.01-1.06), male sex (OR 3.25, 95% CI 1.22-9.32), and more prior ITP therapies (OR 1.42, 95% CI 1.10-1.87). Acute treatment of major bleeds required a median of three treatments (interquartile range [IQR] 2 -4), which included intravenous immune globulin (91% of visits), corticosteroids (78% of visits), and platelet transfusions (75% of visits). Three patients (10%) died, nine (31%) developed recurrent bleeds, one (3%) developed arterial thrombosis, and one (3%) had permanent neurological disability. Six patients presented with minor bleeding and subsequently developed a major bleed after a median of 2 days (IQR 1-3). All six patients had oral purpura and four of six had gross hematuria preceding the major bleed. Conclusions:Major ITP bleeds are associated with significant morbidity and mortality. Oral purpura and hematuria often preceded major bleeds. Further research is needed to refine the definition of a major ITP bleed and develop evidence-based treatment strategies.

Our audit demonstrates a lack of compliance with IVIG Request Form requirements, a lack of documentation of diagnostic criteria and efficacy, and suggests inappropriate use of IVIG. Current implementation of the form may not be sufficient as a strategy for improving appropriate IVIG use.

Patients with muscular temporomandibular disorder (TMD) present with abnormal oxygenation of the jaw muscles. Nonetheless, the deoxygenation pattern of jaw muscles of healthy subjects with frequent wake-time tooth-clenching episodes, who are at greater risk for TMD, has never been investigated. This case-control study compared the deoxygenation of the masseter during standardized tasks between TMD-free individuals with frequent self-reports of wake-time clenching and those with infrequent self-reports. University students ( N = 255) filled out the Oral Behavior Checklist. Fourteen females with high versus low scores—high parafunctional (HP) group ( n = 7, ≥80th percentile of score distribution) versus low parafunctional (LP) group ( n = 7, ≤20th percentile)—completed 2 sessions during which they clenched at their maximum voluntary contraction (MVC) for 2 min and at 10% to 20% MVC for 20 min. Tissue oxygen saturation (StO2) and changes in oxygenated hemoglobin, deoxygenated hemoglobin, and total hemoglobin of the masseter were measured via near-infrared spectroscopy and analyzed with a generalized mixed effect model. A significant interaction effect (task × study group) was found on all outcome measures, indicating that the deoxygenation pattern of the HP group differed from the LP group (all P < 0.001). MVC of the masseter induced an almost 5-times-greater reduction of StO2 in the HP group as compared with the LP group ( P = 0.023). However, the relative increase in StO2 at rest after the MVC was similar between groups ( P > 0.05). At the end of the prolonged MVC task (10% to 20%), the blood flow (change in total hemoglobin) was almost 6 times higher in the LP group as compared with baseline. On the contrary, it increased minimally in the HP group (all P < 0.001). Healthy individuals at risk for TMD have abnormalities in masseter deoxygenation. Future prospective studies are needed to test whether this contributes to the onset of muscular TMD.

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