Optimizing Discharge Summaries: A Multispecialty, Multicenter Survey of Primary Care Clinicians.

BACKGROUND: Patient care in the United States has become increasingly more fragmented, and the discharge summary serves as a critical tool for transmitting information on a patient's hospital admission to the primary care clinician. Some guidelines regarding how to write discharge summaries exist, but few are focused on prioritizing content that is most important to optimize a patient's transition of care. METHODS: We conducted a national survey across various medical primary care specialties, including trainees and advanced practice providers, to understand the priorities of primary care clinicians. We distributed the survey to 2184 clinicians affiliated with 8 large academic institutions. Our response rate was 21%. RESULTS: Hospital course, discharge diagnoses, medication reconciliation, and follow-up sections were ranked as the most important categories with a 95.5% concordance rate among surveyed institutions. The least important sections were contact numbers for inpatient clinicians, ancillary services, weight-bearing status, and wound care. Similar themes were also identified via consensus review of the free-texted comments, adding that discharge summary style was also important. Other identified barriers to high-quality transition of care are both the limited time primary care clinicians can spend reviewing discharge summaries and lack of adequate communication between hospitalists and the outpatient clinician. CONCLUSIONS: High-yield content should be presented at the beginning of the discharge summary and conveyed in a brief, succinct manner to ensure maximal utility of the document as a transition of care tool.

Postacute Sequelae of SARS-CoV-2 Infection and Impact on Quality of Life 1-6 Months After Illness and Association With Initial Symptom Severity.

BACKGROUND: Individuals with coronavirus disease 2019 (COVID-19) may have persistent symptoms following their acute illness. The prevalence and predictors of these symptoms, termed postacute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; PASC), have not been fully described. METHODS: Participants discharged from an outpatient telemedicine program for COVID-19 were emailed a survey (1-6 months after discharge) about ongoing symptoms, acute illness severity, and quality of life. Standardized telemedicine notes from acute illness were used for covariates (comorbidities and provider-assessed symptom severity). Bivariate and multivariable analyses were performed to assess predictors of persistent symptoms. RESULTS: Two hundred ninety patients completed the survey, of whom 115 (39.7%) reported persistent symptoms including fatigue (n = 59, 20.3%), dyspnea on exertion (n = 41, 14.1%), and mental fog (n = 39, 13.5%), among others. The proportion of persistent symptoms did not differ based on duration since illness (<90 days: n = 32, 37.2%; vs >90 days: n = 80, 40.4%; P = .61). Predictors of persistent symptoms included provider-assessed moderate-severe illness (adjusted odds ratio [aOR], 3.24; 95% CI, 1.75-6.02), female sex (aOR, 1.99; 95% CI, 0.98-4.04; >90 days out: aOR, 2.24; 95% CI, 1.01-4.95), and middle age (aOR, 2.08; 95% CI, 1.07-4.03). Common symptoms associated with reports of worse physical health included weakness, fatigue, myalgias, and mental fog. CONCLUSIONS: Symptoms following acute COVID-19 are common and may be predicted by factors during the acute phase of illness. Fatigue and neuropsychiatric symptoms figured prominently. Select symptoms seem to be particularly associated with perceptions of physical health following COVID-19 and warrant specific attention on future studies of PASC.

Prolonged Symptoms After COVID-19 Infection in Outpatients.

We review 127 encounters for polymerase chain reaction-confirmed coronavirus disease 2019 (COVID-19) infection at a multidisciplinary outpatient clinic. We describe the symptomatology, time course, exam, and radiographic findings in this population. Patients with COVID-19 can experience persistent symptoms, primarily respiratory in nature, which can be severe enough to warrant hospitalization.

Gene expression profiles of mouse retinas during the second and third postnatal weeks.

Mouse retina undergoes crucial changes during early postnatal development. By using Affymetrix microarrays, we analyzed gene expression profiles of wild-type 129SvEv/C57BL/6 mouse retinas at postnatal days (P) 7, 10, 14, 18, and 21 and found significantly altered expression of 355 genes. Characterization of these 355 genes provided insight into physiologic and pathologic processes of mouse retinal development during the second and third postnatal weeks, a period that corresponds to human embryogenesis between weeks 12 and 28. These genes formed 6 groups with similar change patterns. Among the genes, sixteen cause retinal diseases when mutated; most of these 16 genes were upregulated in retina during this period. Using the PathArt program, we identified the biological processes in which many of the 355 gene products function. Among the most active processes in the P7-P21 retina are those involved in neurogenesis, obesity, diabetes type II, apoptosis, growth and differentiation, and protein kinase activity. We examined the expression patterns of 58 genes in P7 and adult retinas by searching the Brain Gene Expression Map database. Although most genes were present in various cell types in retinas, many displayed high levels of expression specifically in the outer nuclear, inner nuclear, and/or ganglion cell layers. By combining our 3 analyses, we demonstrated that during this period of mouse retinal development, many genes play important roles in various cell types, multiple pathways are involved, and some genes in a pathway are expressed in coordinated patterns. Our results thus provide foundation for future detailed studies of specific genes and pathways in various genetic and environmental conditions during retinal development.

Distinct gene expression profiles and reduced JNK signaling in retinitis pigmentosa caused by RP1 mutations.

To understand the mechanisms underlying autosomal dominant progressive retinitis pigmentosa (RP) caused by the mutations of the RP1 gene and to identify molecules that play roles in the early disease process, we used Affymetrix U74Av2 microarrays to compare the gene expression profiles of retinas from Rp1-/- and Rp1+/+ mice at postnatal days (P) 7, 10, 14, 18 and 21. These profiles were independently verified by comparison with results of retinal serial analysis of gene expression, U74Av2 array studies of mouse retinas, real-time PCR and in situ hybridization. We found that the disruption of Rp1 significantly affected the expression of multiple clusters of genes whose products were involved in diverse biological pathways. The molecular responses to the disruption of Rp1 changed dramatically during development and were distinct from responses to the disruption of photoreceptor transcription factors (Crx-/- or Nrl-/-) and a phototransduction molecule (Pde6brd1). We found specific alterations of gene expression in the c-Jun N-terminal kinase (JNK) signaling cascades. Western analysis confirmed that the phosphorylation of key members in the JNK signaling cascades (i.e. JNK1, JNK2, MAP2, MKK4 and c-Jun) is reduced, whereas phospho-ERK and phospho-p38 are unchanged, in Rp1-/- retinas at P18-21. Immunostaining demonstrated that, like Rp1, phospho-JNKs and phospho-MAP2 are present in outer segments of photoreceptors. Our studies reveal unique molecular phenotypes in multiple biological pathways and the specific reduction of JNK signaling cascades in RP1 diseases, and suggest that RP1, a doublecortin-containing microtubule associated protein, and JNK signaling cascades play integral roles in photoreceptor development and maintenance. Our studies further suggest JNK-related therapeutic strategies for RP1 diseases.

Purkinje cell degeneration (pcd) phenotypes caused by mutations in the axotomy-induced gene, Nna1.

The classical recessive mouse mutant, Purkinje cell degeneration (pcd), exhibits adult-onset degeneration of cerebellar Purkinje neurons, retinal photoreceptors, olfactory bulb mitral neurons, and selected thalamic neurons, and has defective spermatogenesis. Here we identify Nna1 as the gene mutated in the original pcd and two additional pcd alleles (pcd2J and pcd3J). Nna1 encodes a putative nuclear protein containing a zinc carboxypeptidase domain initially identified by its induction in spinal motor neurons during axonal regeneration. The present study suggests an unexpected molecular link between neuronal degeneration and regeneration, and its results have potential implications for neurodegenerative diseases and male infertility.