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Hypercholesterolemia Induced by a High-Fat, Low-Carbohydrate Diet in a 16-year-old Male and 6-year-old Female.
No full textBackground: The ketogenic diet is a high-fat, low-carbohydrate (HFLC) diet that has been linked to hypercholesterolemia. There are ongoing studies on the connection between hypercholesterolemia and adherence to the ketogenic diet. Medically supervised HFLC ketogenic diets with up to 90% fat have been used successfully in children as an alternative treatment for epilepsy. Although safety and efficacy data are limited in children, this high-fat diet has also been used for weight loss. Case information: Patient 1:A 16-year-old previously healthy African American male was concerned about his weight and his mother started him on a ketogenic diet. Before diet implementation, he weighed 93.2 kg (BMI of 31.6 kg/m2; 99%) and had a low-density lipoprotein cholesterol (LDL-C) of 114 mg/dL (normal LDL-C is below 110 mg/dL). During the following months, the patient lost weight and his LDL-C levels continuously increased and peaked at 348 mg/dL after losing 59lbs on the ketogenic diet. The patient was offered pharmacotherapy but the parents declined. During his most recent follow-up appointment, the patient stopped adhering to the ketogenic diet and increased his weight to 79.2 kg (BMI of 26.2 kg/m2; 87.5%), and his LDL-C level dropped to 182 mg/dL. Throughout appointments, triglycerides remained normal. No pathological variants for APOB, LDLR, LDLRAP1, and PCSK9were found on genetic testing. Patient 2: A 6-year-old female with a history of idiopathic ketotic hypoglycemia and growth hormone deficiency was started on the ketogenic diet as a way to help control hypoglycemic episodes. The diet helped keep her blood glucose levels stable but she demonstrated severe hypercholesterolemia on her lipid screening. Her LDL-C levels were significantly elevated at 310 mg/dL 37 months after her first appointment. She was taken off the ketogenic diet for 6-8 weeks with significant improvement in her LDL-C dropping down to 116 mg/dL. At 42 months, the patient was admitted to the hospital for hypoglycemia. It was noted that the mother had started the patient on the ketogenic diet again due to recurrent episodes of hypoglycemia. On lipid screening, her LDL-C was back up to 397 mg/dL. Genetic testing for APOB, LDLR, LDLRAP1, and PCSK9 were all negative. Conclusions: Several mechanisms have been proposed to explain the adverse effect of hypercholesterolemia in individuals participating in the ketogenic diet. This includes increased saturated fatty acid intake causing downregulation of LDL receptors, genetic polymorphisms, and cholesterol mobilization associated with weight loss. Although there is ongoing research regarding the mechanism behind hypercholesterolemia associated with HFLC diets, there is no clear, definitive explanation yet. Our case study and other case series in adults on the ketogenic diet for weight loss show the importance of ruling out HFLC diets when patients present with hypercholesterolemia and have no known genetic mutations suggesting familial hypercholesterolemia (FH)
Perioperative Complications in Swan Neck Deformity Repair Case Report
No full textBackground
Excessive vagal stimulation in the intraoperative and perioperative periods can lead to bradycardia, asystole, and death. Painful stimulus or excessive pressure on the vagus nerve can lead to bradycardia. Increased stretch from a mechanical standpoint can also lead to more vagal nerve firing and input.
Case Summary
This case investigates the disease process of a 69-year-old female who presented to the surgical team following multiple failed conservative treatments for cervical chin on chest spinal deformity, requiring three months of hospitalization. Given the expected airway edema and swallowing dysfunction, surgical risks were high, and the patient was informed of potential complications. She consented for surgery and was educated on risks and benefits, including the possibility of requiring a tracheostomy and a Percutaneous Endoscopic Gastrostomy placement. The patient underwent a closed reduction of cervicothoracic spinal deformity, anterior cervical C4-5 osteotomy, C4-C7 corpectomies, C3-T1 anterior cervical fusion, posterior cervical C5-6 osteotomy, C2-T6 laminectomies, posterior cervical instrumented fusion C2-T8, and left L4 hemilaminectomy for placement of drains. On post op day 6, the patient requested PEG and tracheotomy placement. On post op day 10, the patient compounded a necrotizing soft tissue infection of the anterior neck that required emergent washout. The wound displayed profuse black fluid upon incision which along with imaging and crepitus on physical exam led to the diagnosis of acute necrotizing fasciitis. The patient also acquired persistent cervical esophageal perforation with a non-healed fistula and was taken to the OR two days later for tracheotomy revision and esophageal perforation repair. On post op day 20, the patient developed a neck hematoma requiring OR incision and drainage. On post op day 30, the patient was being turned by nursing to clean cervical wounds and became unresponsive. The patients became bradycardic, then developed asystole with no palpable pulses. After a few seconds, telemetry showed sinus rhythm and vitals became stable. Cardiology was consulted and attributed the patient’s episodes of asystole to pressure on the carotid sinus causing stimulation of the vagus nerve. The care team was instructed to minimize turning the patient to avoid further asystole. Local anesthesia was advised for future procedures. With an arrhythmia lasting longer than 90 seconds, pacemaker placement was indicated and performed.
Discussion
The interprofessional team effort allowed us to quickly identify the cause and treatment, which were vagal nerve compression and pacemaker placement, respectively. There are several explanations as to what contributed to the vagal stimulation. These include anatomical reconstruction, postoperative infection, neck hematoma, esophageal perforation, or mechanical ventilation stimulation. These may have caused vagal nerve stretching, causing increased vagal sensitivity. Above all, the increased vagal stimulation mostly occurred due to the drastic change in the patient’s anatomy, going from an extreme hyper flexed cervical position to hyperextension. This causes stretching and pulling on the structures in that region, which includes the vagus nerve. As anesthesia providers, it is crucial to recognize these possible complications and be able to adapt to care for these patients inside and outside of the operating room
Impact of gross anatomy review on ultrasound learning in first-year medical students: A pilot study
No full textIntroduction: Ultrasound (US) integration in undergraduate medical education (UME) has been a popular topic for the past decade. Current literature indicates ultrasound inclusion in UME is commonly integrated in gross anatomy instruction or clinical skills courses. US inclusion in gross anatomy focuses on overall anatomy understanding, whereas US in clinical skills courses focuses on the diagnostic application of medical imaging. Although there is plenty of literature demonstrating the benefits of US inclusion in gross anatomy, there is little research looking at the use of gross anatomy reviews prior to learning clinical ultrasound. Further, there is little research investigating how transferable gross anatomy identification is to ultrasound anatomy identification. Therefore, this study's purpose is to assess the effects of gross anatomy review prior to learning clinical ultrasound.
Methods: 22 first year medical students interested in joining the ultrasound interest group (USIG), an extracurricular student group, participated in the study in the spring semester of 2023. There were four ultrasound imaging modules taught during the semester: cardiopulmonary, liver/biliary, E-fast, and musculoskeletal. Students were divided into two groups where they were required to participate in a pre-module quiz, attend the ultrasound instruction, then complete a post-module quiz and survey after the ultrasound instruction. The EXP group had to participate in an additional anatomy review prior to the ultrasound instruction session. Pre- and post-module quizzes contained gross anatomy structures of the relevant anatomy for the module, along with paired ultrasound images of that anatomical structure. The quizzes for each module were identical to each other allowing repeated measures. This allows for tracking students ability to transfer knowledge from gross anatomy identification to ultrasound anatomy identification. Groups switched treatments for each module, allowing equal exposure to both treatments. Quiz scores were compared within and between groups, setting significance level at p<0.05.
Results: Both CON and EXP groups significantly improved in their performance from pre-quiz to post-quiz in all four sub-scores for Module 1 (p<.001 for overall; d=1.3, US; d=1.16 and transfer; d=1.34, p<.05 for anatomy; d=.51) and Module 4 (p<.001 for overall; d=1.1,and transfer; d=.74, p<.01 for anatomy; d=.67, and US; d=1.47). Significant increases were seen in three sub-scores for module 2 (p<.01 for overall; d=.77, and US; d=.65, p<.05 for transfer; d=.46). There were no significant increases in performance from pre-quiz to post-quiz in module 3. Looking at self-improvement between groups, the EXP group did show higher mean gains than the CON group and mild to moderate effect sizes, although these comparisons were not significant. The EXP group showed higher mean scores on post-quiz assessments for most sub-scores, including mild to moderate effect sizes, although none of these were significant.
Conclusion: Ultrasound is a valuable tool in all areas of medicine, especially in anatomy learning. This study shows that a gross anatomy review does have a positive impact on student performance when learning US. Medical students learning US may receive benefit from a gross anatomy review to reintroduce previously learned material and further reinforce US instruction.N
Addressing Disparities in Treatment for Substance Use Disorder Among Individuals with Developmental Disabilities: Perspectives from Treatment Facility Employees
No full textPurpose
Research on substance use disorder (SUD) among individuals with developmental disabilities (DD) is limited. The extant literature suggests that people with DD are less likely to use substances overall compared to people without a disability; however, they are more susceptible to SUD if they do use substances. Among facilities in the United States that provide aid for individuals with DD and treatment facilities for individuals with SUD, there are currently no interdisciplinary practice guidelines or training materials available for providers treating those with a co-diagnosis of DD and SUD. Our project aims to reduce the disparities between treatment guidelines and materials available for people with a co-diagnosis of both SUD and DD. The purpose of this analysis was to gauge overall awareness of providing treatment for individuals with SUD/DD co-diagnosis and reflect on current protocols regarding this population.
Methods
In this project, interviews were conducted with workers at facilities that primarily provide SUD services. Relevant facilities were identified and selected through systematic internet searches. In this study, 11 questions were asked to workers at facilities through 15-30 minute phone interviews. Questions that were used for this analysis revolved around themes of workers’ perspectives on the importance of integrating SUD/DD services, their current practices, and their future recommendations for integrating care for individuals with both SUD/DD.
Results
We conducted a total of 12 interviews. Responses came from the South and Midwest United States geographical regions. From these interviews, we found that most programs aim to individualize their approaches to treating this specific population. However, there is no standardized approach to how they individualize these cases. Furthermore, many programs expressed that they rarely refer individuals with a co-diagnosis of SUD/DD outside of their agency and feel inadequately prepared to treat individuals with SUD/DD co-diagnosis, which further emphasizes the need for accessible standardized guidelines. Overall, many workers expressed a need for improved access to screenings, assessment tools, specific guidelines, knowledge, training, and specialized programs for the variety of specific types of DDs.
Conclusions
People with DD that experience SUD are a vulnerable population with few resources. To meet the needs of this vulnerable population, standardized guidelines and training materials should be developed to address the specific needs of this patient population and equip healthcare providers and stakeholders with the tools necessary to ensure this population has proper and equitable access to treatment.Texas Council for Developmental Disabilitie
Cerebrovascular disease is associated with Alzheimer's plasma biomarker concentrations in adults with Down syndrome
No full textBy age 40 years, over 90% of adults with Down syndrome have Alzheimer's disease pathology and most progress to dementia. Despite having few systemic vascular risk factors, individuals with Down syndrome have elevated cerebrovascular disease markers that track with the clinical progression of Alzheimer's disease, suggesting a role of cerebrovascular disease that is hypothesized to be mediated by inflammatory factors. This study examined the pathways through which small vessel cerebrovascular disease contributes to Alzheimer's disease-related pathophysiology and neurodegeneration in adults with Down syndrome. One hundred eighty-five participants from the Alzheimer's Biomarkers Consortium-Down Syndrome [mean (SD) age = 45.2 (9.3) years] with available MRI and plasma biomarker data were included in this study. White matter hyperintensity (WMH) volumes were derived from T2-weighted fluid-attenuated inversion recovery MRI scans, and plasma biomarker concentrations of amyloid beta 42/40, phosphorylated tau 217, astrocytosis (glial fibrillary acidic protein) and neurodegeneration (neurofilament light chain) were measured with ultrasensitive immunoassays. We examined the bivariate relationships of WMH, amyloid beta 42/40, phosphorylated tau 217 and glial fibrillary acidic protein with age-residualized neurofilament light chain across Alzheimer's disease diagnostic groups. A series of mediation and path analyses examined statistical pathways linking WMH and Alzheimer's disease pathophysiology to promote neurodegeneration in the total sample and groups stratified by clinical diagnosis. There was a direct and indirect bidirectional effect through the glial fibrillary acidic protein of WMH on phosphorylated tau 217 concentration, which was associated with neurofilament light chain concentration in the entire sample. Amongst cognitively stable participants, WMH was directly and indirectly, through glial fibrillary acidic protein, associated with phosphorylated tau 217 concentration, and in those with mild cognitive impairment, there was a direct effect of WMH on phosphorylated tau 217 and neurofilament light chain concentrations. There were no associations of WMH with biomarker concentrations among those diagnosed with dementia. The findings from this cross-sectional study suggest that among individuals with Down syndrome, cerebrovascular disease promotes neurodegeneration by increasing astrocytosis and tau pathophysiology in the presymptomatic phases of Alzheimer's disease, but future studies will need to confirm these associations with longitudinal data. This work joins an emerging literature that implicates cerebrovascular disease and its interface with neuroinflammation as a core pathological feature of Alzheimer's disease in adults with Down syndrome.This work was supported by the US National Institutes of Health (NIH) grants RF1 AG079519, U19 AG068054, U01 AG051412, U01 AG051406, and F31 AG090091
Temporal Dynamics of Mitochondrial Dysfunction and Retinal Ganglion Cell Degeneration Following Endothelin-1 Exposure
No full textPurpose: Endothelin-1 (ET-1) and its receptors have been identified as upregulated factors in the aqueous humor and retina of animal models with glaucoma, implicating them in the pathogenesis of glaucomatous neurodegeneration. This study aims to investigate the effects of ET-1 on mitochondrial morphology, a key aspect of cellular health.
Methods: C57BL/6J mice (13 weeks old) received intravitreal injections of either ET-1 or vehicle (water) in both eyes 24 hours, 72 hours, or 7 days before collection. One eye was used for retinal flat mounts stained with RBPMS to quantify retinal ganglion cells (RGCs), while the other eye was processed for transmission electron microscopy after paraffin embedding. Optic nerves were sectioned, and ten images were captured per nerve section. Mitochondria within optic nerve axons were enumerated and graded based on cristae appearance (with grades ranging from 1 to 5). Comparisons between vehicle and ET-1 treated eyes at each time point were performed for mitochondrial scores and counts (Mann-Whitney test, n=4 per group). Cell counts from retinal flat mounts were compared across groups and time points (Student’s T Test).
Results: Significant RGC loss was observed in the peripheral and mid-peripheral retina 24 hours post ET-1 injection (P=0.01 and 0.04 respectively), with the disparity between vehicle and ET-1 treatments diminishing at later time points. While a trend towards reduced mitochondrial numbers in optic nerve axons post ET-1 injection was noted across all time points, significance was not reached. Mitochondrial health scores were notably diminished at 24 hours post-injection in both vehicle and ET-1 treated groups, with ET-1 demonstrating appreciable damage to mitochondria at 72 hours compared to vehicle-injected animals. However, mitochondrial health improved over time in the ET-1 treated group, with no discernible differences observed at 7 days.
Conclusion: The acute decline in mitochondrial morphology following intravitreal injection of both ET-1 and vehicle suggests induced cellular stress. However, ET-1 injection led to immediate cell death not observed in the vehicle-injected cohort. While mitochondrial morphology swiftly recovered in the vehicle-injected group, ET-1 administration prolonged mitochondrial damage. These alterations in mitochondrial morphology may impair mitochondrial energy production efficiency, potentially contributing to retinal ganglion cell vulnerability in glaucoma.NIH EY028179, NIH T32AG02049
Long-term Follow-up of Hip Resurfacing Arthroplasty Patients: A Comprehensive Review of Outcomes Over 15 Years
No full textPurpose: Hip resurfacing arthroplasty (HRA) has emerged as a promising alternative to total hip arthroplasty (THA) for managing severe osteoarthritis, especially in younger, active males seeking a return to high impact activities. While short to medium-term follow-up studies have demonstrated favorable clinical outcomes and survival rates, there is increasing interest in the long-term durability of HRA, in terms of implant survivorship and patient outcomes and attitudes. The existing body of literature on HRA longevity is predominantly limited to follow-up periods of up to 10 years. As such, the purpose of this study was to evaluate the long-term survivorship of HRA with a minimum follow-up period of fifteen years.
Methods: A retrospective review of hip resurfacing arthroplasties performed by a single surgeon at a high-volume surgical center between 2006-2008 was conducted. Given that the majority of these patients were male, we elected to focus exclusively on male patients to control for potential confounding factors related to sex and standardize our findings. Patient demographics were collected including age, BMI, and laterality. Patient reported outcome measures (PROMs) including Hip Disability and Osteoarthritis Outcome Score, Joint Replacement (HOOS-JR), Harris Hip Score (HHS), Visual Analogue Scale (VAS), and UCLA Activity Scores were collected at fifteen years post-operation. Subject satisfaction surveys were also collected, and Kaplan-Meier survival analyzed implant revisions.
Results: A total of 312 patients (369 hips) out of 470 (543 hips) with a minimum 15-year follow up were included in this study, representing a follow-up rate of 66.4%. The mean age at surgery was 50.5 ± 7.8 years and the mean BMI was 27.9 ± 4.3 kg/m2. The mean scores for HOOS JR, HHS, VAS, and UCLA activity scores at final follow-up were 97.5 ± 6.7, 96.7 ± 8.3, 0.3 ± 0.9, and 7.9 ± 1.9, respectively. Out of the 369 HRA implants, 24 were revised to total hip arthroplasty, indicating 93.5% survivorship. Excluding patients who required revision, 98.9% of patients expressed satisfaction with the procedure.
Conclusions: Positive outcomes in PROMs and subject satisfaction scores accompanied by high implant survival, indicate that the metal-on-metal HRA procedure exists as a safe and effective solution for end-stage osteoarthritis in young (50.5 ± 7.8 years) male patients at long-term follow-up. Favorable outcomes persisting 15-years after primary procedure suggests that HRA may serve as a viable alternative to THA, its longstanding counterpart, at high-volume centers with proper expertise of the procedure. This avenue warrants further exploration in the future of our study, with potential implications for the optimization of patient care and surgical decision-making in this population
Efficacy of Osteopathic Manipulative Treatment in Post-Stroke Recovery Patients
No full textBackground:
Each year, an estimated 795,000 people report having a stroke. Stroke is the 5th leading cause of death and the 10th leading cause of adult disability in the United States, leading to significant physical impairment.
Stroke patients specifically suffer from pain related to positional changes, muscle contractures, and somatic dysfunctions. Beneficial stroke rehabilitation begins within the first three months following presentation, in the subacute setting. Current literature has primarily addressed pain and musculoskeletal limitations in patients in a post-acute stroke setting.
Case Information:
HPI: A 53 y/o Caucasian female presented to the emergency department for a 6-hour history of slurred speech and right-sided arm and leg weakness. She suddenly lost the ability to speak and felt right-upper-extremity and right-lower-extremity weakness. She denied any falls or trauma during this period. She reported her speech improved in the ED but had no improvement in her right-sided weakness.
Physical Exam: An examination of her extremities showed a bilateral ulnar deviation of the MCP joints with swan neck deformity and diffuse finger and hand joint enlargement. The musculoskeletal exam showed her LUE and LLE had 5/5 strength at all nerve roots. Her RUE only had limited thumb adduction. Her RLE had 0/5 strength. The neurological exam showed right-sided facial muscle weakness; otherwise, the patient had bilaterally intact cranial nerves. Light touch sensations were intact bilaterally on her upper and lower extremities.
On day 3 of her hospitalization, the osteopathic neuromusculoskeletal medicine (ONMM) hospital service was consulted for generalized whole-body aches with significant pain in her left shoulder and neck. The initial session included the use of counterstrain (CS), balanced ligamentous tension (BLT), and myofascial release (MFR) to help reduce muscle strain and tension.
On day 8, the patient was transferred to the Rehabilitation Unit where she received daily Physical Therapy and Occupational Therapy sessions. Goals of OMT shifted from symptomatic treatment to augmenting the patient’s ability to participate in PT and OT.
Throughout her stay in the Rehabilitation Unit, the patient notified the ONMM team of increased participation in PT and OT and increased movement of her right side. Therapy sessions lead to right-sided pain primarily in her shoulder and knee. OMT was performed daily, focusing on her various right-sided restrictions.
The patient was treated with OMT a total of 14 times across 36 days. The patient reported improvement of pain in all treated regions as well as increased motor function in her paralyzed side.
Conclusions:
Her improvements highlight the importance of early consultation of the ONMM services in post-stroke patients with functional impairment. The case demonstrates that in conjunction with evidence-based PT/OT, subacute stroke OMT can increase biomechanical functionality as demonstrated by the increased functionality of both the paralyzed extremities.
Further research should focus on the use of OMM and other osteopathically informed approaches in stroke rehabilitation as well as the long-term effects of initiating OMT in stroke patients within this subacute window. Studies have demonstrated that the optimal therapeutic window is within the first 3 months following a stroke
Evaluating philtrum-to-tragus distance as an external predictor of nasal passage dimensions: A computed tomography (CT) approach
No full textResearch Appreciation Day Award Winner - School of Biomedical Sciences, 2024 Department of Physiology & Anatomy (Structural Anatomy & Rehabilitation Sciences) Award - 1st PlaceAccurate quantification of nasopharyngeal temperature requires the placement of a flexible intranasal probe into the upper or mid-nasopharynx. Yet, without guidance from medical imaging, data shows that in practice less than half of nasopharyngeal temperature probes are optimally positioned. Still, previous studies have suggested that the distance between the philtrum (external nose) to tragus (external ear) provides a reliable predictor of internal nasal passage dimensions. However, previous attempts to verify the accuracy of this external proxy have returned equivocal results. Accordingly, this study employed measurements collected from CT scans of 11 living participants (4 female, 7 male) to assess associations between external philtrum-tragus length and internal lengths of the nasal cavity, nasopharynx, and total nasal passage (i.e., cavity + pharynx). Results show statistically significant correlations between philtrum-tragus length and internal measurements of nasal cavity (r=0.412, p=0.033) and total nasal passage (r=0.502, p=0.015) length. In contrast, no significant correlation was identified between philtrum-tragus length and nasopharynx length (r=0.110, p=0.320). Despite the small size of the study sample, these suggest that philtrum-tragus length can provide insights for estimating internal dimensions relating to the location of the end of nasal cavity (i.e., choanal aperture) and the posterior wall of nasopharynx. Thus, this external measurement may enhance the accuracy of intranasal probe placement, especially when medical imaging data (i.e., radiographs, CT, MRI) are not available for guidance. Accordingly, additional investigation into the applied utility of philtrum-tragus length with larger sample sizes appears warranted.National Science Foundation #2020506 (Cowgill), #2020096 (Ocobock), #2203808 (Cho), #2020715 (Maddux). North Texas Regional IRB: #1875793-1
The ketogenic diet and hypoxia promote mitophagy in the context of glaucoma
Get PDFMitochondrial homeostasis includes balancing organelle biogenesis with recycling (mitophagy). The ketogenic diet protects retinal ganglion cells (RGCs) from glaucoma-associated neurodegeneration, with a concomitant increase in mitochondrial biogenesis. This study aimed to determine if the ketogenic diet also promoted mitophagy. MitoQC mice that carry a pH-sensitive mCherry-GFP tag on the outer mitochondrial membrane were placed on a ketogenic diet or standard rodent chow for 5 weeks; ocular hypertension (OHT) was induced via magnetic microbead injection in a subset of control or ketogenic diet animals 1 week after the diet began. As a measure of mitophagy, mitolysosomes were quantified in sectioned retina immunolabeled with RBPMS for RGCs or vimentin for Muller glia. Mitolysosomes were significantly increased as a result of OHT and the ketogenic diet (KD) in RGCs. Interestingly, the ketogenic diet increased mitolysosome number significantly higher than OHT alone. In contrast, OHT and the ketogenic diet both increased mitolysosome number in Muller glia to a similar degree. To understand if hypoxia could be a stimulus for mitophagy, we quantified mitolysosomes after acute OHT, finding significantly greater mitolysosome number in cells positive for pimonidazole, an adduct formed in cells exposed to hypoxia. Retinal protein analysis for BNIP3 and NIX showed no differences across groups, suggesting that these receptors were equivocal for mitophagy in this model of OHT. Our data indicate that OHT and hypoxia stimulate mitophagy and that the ketogenic diet is an additive for mitophagy in RGCs. The different response across RGCs and Muller glia to the ketogenic diet may reflect the different metabolic needs of these cell types.The author(s) declare financial support was received for the research, authorship, and/or publication of this article. Research supported by NIH EY-026662 to DI