Cheyenne VA Medical Center

In fiscal year 2020 (FY20), the Veterans Health Administration (VHA) initiated a pilot study to determine whether automated audiometry could be used in conjunction with asynchronous telehealth systems to increase access points for audiologic services to Veterans across multiple VHA locations. Veterans Integrated Service Network (VISN) 19 was provided funding from the Office of Rural Health (ORH) to take on this pilot project to trial a hub-and-spoke model of asynchronous automated audiometry service delivery. With this care model, the patient and trained telepresenter are in one location utilizing the testing equipment, and the results are collected and transmitted to the patient record. The audiologist then reviews the stored results from within the patient record, diagnoses as able based on results, and provides follow-up care to the Veteran via video or telephone visit, at which time a further care plan is developed. Although there were many challenges with the equipment procurement and supply chain in the postpandemic world, 16 of the initial 20 sites across the region were launched by the end of FY24. As a result of this pilot, asynchronous automated audiometry was approved as an Enterprise-Wide Initiative in the VHA system with 34 additional sites across VHA receiving ORH funding and multiple additional sites beginning their own asynchronous automated audiometry programs.

BackgroundHealthcare-associated infections (HAI) have tremendously increased since the coronavirus-19 pandemic. With this increase, various attempts should be made to keep multidrug-resistant organisms in check. In 2021, the Veterans Affairs in San Antonio identified a patient with a multidrug-resistant Acinetobacter baumannii complex (MDR-A). This study was undertaken to determine the temporal and spatial relationship of similarly identified MDR-A from other patients at our facility to help prevent spread. We highlight the role whole-genome sequencing plays in a nosocomial outbreak investigation.MethodsSince the identification of the first MDR-A, we performed interventions to include closure of the unit for new admissions, terminal cleaning, and collection of nasopharyngeal, peri-rectal, urine and wound swabs for surveillance. 15 positive samples were sent from our facility to Multidrug- Resistant Organism Repository and Surveillance Network (MRSN) for genotyping.ResultsGenotyping results confirmed that there were only one to four Single Nucleotide Polymorphism (SNP) variations between three of the patient isolates indicating that these were genetically related with likely nosocomial transmission. All isolates carried an OXA-23 carbapenemase and a 16S rRNA methyltransferase which conferred resistance to all clinically relevant aminoglycosides. Overall, twelve isolates were identified from our facility with < =4 SNP variations interlinking them with prior isolates sent to MRSN. MRSN identified 2-45 SNP variations between 87 isolates from seven different hospitals in South Texas (Figure 1). Environmental sampling in our hospital revealed an Acinetobacter baumannii isolated from shower trolleys. Since the organism isolated was identical, spread was presumed secondary to the contaminated shower trolley.MDR-A cluster indicating interrelation between various isolates from seven different facilities in South Texas.This figure depicts four common isolates pictured in the center, which resulted in SNP variations and spread across seven facilities in South Texas. The SNP variations between isolates are noted here. Several inter-facility spread of MDR-A took place as can be seen here. Abbreviations: SNP, Single Nucleotide Polymorphisms; MDR-A, Multidrug Resistant Acinetobacter baumannii complexConclusionSpread of MDR-A from our index case was linked to transmission from shower trolleys. These were disinfected, and focused disinfection of all high-touch surfaces was undertaken in addition. Further spread was successfully prevented and no other cases with MDR-A identified thereafter. This case highlights the critical steps in outbreak investigation and highlights the importance of whole-genome sequencing in this process.DisclosuresAll Authors: No reported disclosures

Objective: To improve door to thrombolysis time to less than 60 minutes for acute stroke patients in a community hospital with telestroke access. Background: Earlier initiation of thrombolysis (tPA) therapy in acute stroke patients is associated with improved patient outcomes. Delays in the identification and workup of stroke patients can impact thrombolysis treatment time. Methods: A multidisciplinary workgroup was created in 2015. The care of stroke alert patients was observed over several weeks, identifying barriers and delays in treatment. Multiple interventions were implemented utilizing plan-do-study-act (PDSA) cycles. Door-to-tPA (DTT) times were retrospectively collected for patients with final diagnosis of ischemic stroke and monitored monthly using statistical process control charts. Results: Baseline average DTT was 77 minutes. Initiation of a stroke launch pad and revision of the process to obtain CT scans resulted in a significant decrease in average time to CT to 9 minutes, which was sustained, but without subsequent improvement in DTT times. Further interventions to the stroke alert process improved DTT times transiently but performance was not sustainable. Multiple PDSA cycles were carried out targeting various inefficiencies in the process, knowledge gaps amongst staff, and cultural barriers within the ER physicians. DTT times have gradually improved over time, with average DTT of 48 minutes achieved for Jan-June 2018 (Figure 1). The average number of tPA cases per month increased from 1.3 in 2015 to 2.5 in 2017-2018, likely attributable to revisions in the stroke alert process and stroke alert criteria, and staff education. Conclusion: Continuous quality improvement methodology can be utilized to improve door to tPA times in acute stroke patients. This may require multiple PDSA cycles, addressing cultural and educational barriers, as well as continually revisiting the process to ensure sustained performance.

It is imperative to follow the clinical guidelines for abduction deficits to ensure prompt diagnosis of potentially serious etiologies and monitor only those in which a microvascular etiology is most likely. This case reports highlights a rare diagnosis of a malignant tumor of the lacrimal gland presenting as an abduction deficit. Tumors of the lacrimal gland can cause abduction deficits, which may mimic an abducens nerve palsy. Abducens nerve palsies are often encountered by optometrists. This case report highlights the appropriate workup of an abduction deficit and reviews the literature of adenocarcinoma not otherwise specified. A 67-year-old white man was transferred to the optometry clinic with a presumed ischemic abducens palsy. He was found to have an isolated left abduction deficit without vascular risk factors that prompted neuroimaging revealing a mass of the lacrimal gland. After an en bloc resection, a diagnosis of adenocarcinoma not otherwise specified was made. The patient underwent aggressive surgical exenteration followed by radiation. Using the guidelines for evaluation of an abduction deficit, this serious malignancy was diagnosed. An adenocarcinoma not otherwise specified of the lacrimal gland is rare, and there are limited data on its clinical course, prognosis, and treatment. Recurrence and metastases occur at high rates; therefore, prompt diagnosis and aggressive intervention are crucial.

Canine distemper is uncommon in the pet trade in the United States, in large part due to effective vaccines against Canine distemper virus (CDV). This is a report of CDV affecting 24 young dogs of multiple breeds shortly after sale by 2 pet stores in Wyoming during August-October 2010. Cases were diagnosed over 37 days. Diagnosis was established by a combination of fluorescent antibody staining, reverse transcription polymerase chain reaction, negative stain electron microscopy, and necropsy with histopathology. Viral hemagglutinin gene sequences were analyzed from 2 affected dogs and were identical (GenBank accession no. JF283477). Sequences were distinct from those in a contemporaneous unrelated case of CDV in a Wyoming dog (JF283476) that had no contact with the pet store dogs. The breeding property from which the puppies originated was quarantined by the Kansas Animal Health Department. Puppies intended for sale were tested for CDV. Canine distemper was diagnosed on site in November 2010. At that point 1,466 dogs were euthanized to eliminate dispersal of the disease through commercial channels. The investigation underscores the risks inherent in large-scale dog breeding when vaccination and biosecurity practices are suboptimal.

Deletions of the 22q11.2 region distal to the 22q11.21 microdeletion syndrome region have recently been described in individuals with mental retardation and congenital anomalies. Because these deletions are mediated by low-copy repeats (LCRs), located distal to the 22q11.21 DiGeorge/velocardiofacial microdeletion region, duplications are predicted to occur with a frequency equal to the deletion. However, few microduplications of this region have been reported. We report the identification of 18 individuals with microduplications of 22q11.21-q11.23. The duplication boundaries for all individuals are within LCRs distal to the DiGeorge/velocardiofacial microdeletion region. Clinical records for nine subjects reveal shared characteristics, but also several examples of contradicting clinical features (e.g. macrocephaly versus microcephaly and upslanting versus downslanting palpebral fissures). Of 12 cases for whom parental DNA samples were available for testing, one is de novo and 11 inherited the microduplication from a parent, three of whom reportedly have learning problems or developmental delay. The variable phenotypes and preponderance of familial cases obfuscate the clinical relevance of the molecular data and emphasize the need for careful parental assessments and clinical correlations.

The American Academy of Pediatrics recently removed nicotine from the category of drugs contraindicated during breastfeeding. Little evidence demonstrates that infants exposed to nicotine through breastfeeding experience increased health risks beyond the airborne risks associated with passive smoking. The purpose of this longitudinal, five-week, quasi-experimental pilot study was to determine whether “smoking hygiene,” an educational intervention, reduces the frequency of respiratory symptoms experienced by infants whose mothers both smoke and breastfeed. Twenty-nine mother-infant pairs entered the study with 28% dropping out. Of the 21 mother-infant pairs who completed the study, 66% of the nine infants in the control group experienced respiratory illness, compared to 42% of the 12 infants in the intervention group (x2 = .814; p mt .05). Thus, the difference was statistically nonsignificant in this small sample, but the trend worsened the anticipated direction. The study demonstrates some of the difficulties of intervening with this group of mothers.

To report a case of possible severe, life-threatening thrombocytopenia associated with trimethoprim/sulfamethoxazole (TMP/SMX) therapy. A 54-year-old white woman received a 10-day course of TMP/SMX for treatment of chronic sinusitis. One day after finishing the course of TMP/SMX therapy, the presented to the emergency department because of the development of scattered petechiae on both hands and blood blisters in her mouth. On admission, her complete blood cell count results revealed a severely low platelet count of 2 x 10(3)/mm3. Other laboratory test results were normal, except for elevated blood glucose (nonfasting blood glucose). TMP/SMX was believed to be the most likely cause of thrombocytopenia. She was treated successfully with a transfusion of 2 units of platelets and oral prednisone. Her platelet count increased to 110 x 10(3)/mm3 4 days after discontinuation of TMP/SMX. She was discharged on hospital day 5. On follow-up (2 wk after hospital discharge), her platelet count was normal (351 x 10(3)/mm3). TMP/SMX has been implicated as a cause of thrombocytopenia, which is defined as platelet count < 150 x 10(3)/mm3. Although it is uncommon, spontaneous severe bleeding may occur when platelet count decreases to < or = 10 x 10(3)/mm3. Thrombocytopenia associated with TMP/SMX appears to be an immune-mediated process resulting in platelet destruction by drug-dependent platelet antibodies. Treatment of thrombocytopenia associated with TMP/SMX therapy includes discontinuation of the offending drug and the use of corticosteroids. Platelet transfusion and intravenous immunoglobulin may be required in some patients. Thrombocytopenia associated with TMP/SMX therapy can be serious or life threatening because it may result in significant bleeding complications. This hematologic adverse effect of TMP/SMX may occur even with the usual recommended dosage and duration of therapy. Careful monitoring of complete blood cell count, including platelet count, before and during TMP/SMX therapy is suggested.