Acoustic startle response (ASR) is a defensive reflex that is largely ignored unless greatly exaggerated. ASR is suppressed after moderate and severe traumatic brain injury (TBI), but the effect of mild TBI (mTBI) on ASR has not been investigated. Because the neural circuitry for ASR resides in the pons in all mammals, ASR may be a good measure of brainstem function after mTBI. The present study assessed ASR in Sprague-Dawley rats after mTBI using lateral fluid percussion and compared these effects to those on spatial working memory. mTBI caused a profound, long-lasting suppression of ASR. Both probability of emitting a startle and startle amplitude were diminished. ASR suppression was observed as soon as 1 day after injury and remained suppressed for the duration of the study (21 days after injury). No indication of recovery was observed. mTBI also impaired spatial working memory. In contrast to the suppression of ASR, working memory impairment was transient; memory was impaired 1 and 7 days after injury, but recovered by 21 days. The long-lasting suppression of ASR suggests long-term dysfunction of brainstem neural circuits at a time when forebrain neural circuits responsible for spatial working memory have recovered. These results have important implications for return-to-activity decisions because recovery of cognitive impairments plays an important role in these decisions.

Background Infection with the novel severe acute respiratory syndrome coronavirus 2 has been associated with a hypercoagulable state. Emerging data from China and Europe have consistently shown an increased incidence of venous thromboembolism (VTE). We aimed to identify the VTE incidence and early predictors of VTE at our high-volume tertiary care center. Methods We performed a retrospective cohort study of 147 patients who had been admitted to Temple University Hospital with coronavirus disease 2019 (COVID-19) from April 1, 2020 to April 27, 2020. We first identified the VTE (pulmonary embolism [PE] and deep vein thrombosis [DVT]) incidence in our cohort. The VTE and no-VTE groups were compared by univariable analysis for demographics, comorbidities, laboratory data, and treatment outcomes. Subsequently, multivariable logistic regression analysis was performed to identify the early predictors of VTE. Results The 147 patients (20.9% of all admissions) admitted to a designated COVID-19 unit at Temple University Hospital with a high clinical suspicion of acute VTE had undergone testing for VTE using computed tomography pulmonary angiography and/or extremity venous duplex ultrasonography. The overall incidence of VTE was 17% (25 of 147). Of the 25 patients, 16 had had acute PE, 14 had had acute DVT, and 5 had had both PE and DVT. The need for invasive mechanical ventilation (adjusted odds ratio, 3.19; 95% confidence interval, 1.07-9.55) and the admission D-dimer level ≥1500 ng/mL (adjusted odds ratio, 3.55; 95% confidence interval, 1.29-9.78) were independent markers associated with VTE. The all-cause mortality in the VTE group was greater than that in the non-VTE group (48% vs 22%; P = .007). Conclusion Our study represents one of the earliest reported from the United States on the incidence rate of VTE in patients with COVID-19. Patients with a high clinical suspicion and the identified risk factors (invasive mechanical ventilation, admission D-dimer level ≥1500 ng/mL) should be considered for early VTE testing. We did not screen all patients admitted for VTE; therefore, the true incidence of VTE could have been underestimated. Our findings require confirmation in future prospective studies.

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Patient: Female, 68-year-old Final Diagnosis: Sarcoidosis Symptoms: Dysphagia • epigastric pain • nausea • vomiting Medication: — Clinical Procedure: — Specialty: Gastroenterology and Hepatology Objective: Rare disease Background: Sarcoidosis is a multisystem granulomatous disease with predominant pulmonary involvement and rare gastrointestinal (GI) involvement. The stomach is the most common site when there is GI involvement. Symptomatic gastric sarcoidosis with biopsy-proven disease has rarely been reported and much of the knowledge is from case reports involving white patients. Case Report: Our unique case involves a flare of gastric sarcoid in an African American patient with biopsy-proven disease and we highlight our unique broad, multidisciplinary treatment approach that has not been described previously. A 68-year-old woman with pulmonary sarcoidosis presented with epigastric pain, nausea, vomiting, and dysphagia. The diagnosis of gastric sarcoid was made several years prior based on an upper endoscopy biopsy showing non-caseating granulomas in the antrum. She had previously experienced minimal relief of gastric symptoms with corticosteroids. In addition to a steroid taper, the patient experienced improvement in symptoms with a PPI (proton pump inhibitor), bowel regimen, and speech therapy techniques. Conclusions: Gastric symptoms can be a presenting sign for a sarcoid flare in a patient with pulmonary sarcoidosis, which is important for both pulmonologists and gastroenterologists to recognize. In addition to traditional therapy with corticosteroids, our unique broader, multidisciplinary approach with PPI, bowel regimen, and speech therapy techniques such as a liquid wash are important components of treatment for gastric sarcoid that have not been described in previous case reports.

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