United States

Background
Tractional retinal detachment (TRD) is a severe complication of diabetic retinopathy, but its risk factors and impact on mortality in patients with Type I (T1DM) and Type II (T2DM) diabetes remain underexplored. Given the rising prevalence of diabetes, understanding the key contributors to TRD development is critical. This study aims to identify risk factors for TRD and evaluate its effect on survival in individuals with T1DM and T2DM.
Methods
A retrospective study was conducted using the US TriNetX Network database, identifying adults with T1DM and T2DM who were diagnosed with TRD between 2010-2024. Baseline characteristics, including demographics, comorbidities, renal and glycemic labs, and use of antidiabetic medications, were collected within 1 year of diagnosis. Propensity score matching (PSM) of these characteristics was performed to compare T2DM patients with and without TRD, and the same analysis was repeated for T1DM patients. Data were expressed as n (%) or mean (standard deviation). The primary outcome was all-cause mortality over 10 years, analyzed with Kaplan-Meier curves and log-rank tests.
Results
Among 14,701 adults with TRD, 9,820 (66.8%) had T2DM and 3,903 (26.5%) had T1DM. Compared to T2DM patients without TRD (n=3,897,132), the T2DM and TRD cohort had a higher prevalence of Black race (3,172 [32.3%]), HTN (4,624 [47.1%]), adverse SDOH (176 [1.8%)]), higher A1c (8.4 [2.3]%), lower eGFR (53.0 [36.7] mL/min), and higher CRP (42.4 [68.2] mg/L) (p&lt;0.001 for all). Similarly, the T1DM and TRD cohort exhibited higher prevalence of Black race (1,288 [33.0%]), smoking (68 [1.8%]), HTN (2,277 [58.4%]), adverse SDOH (108 [2.8%]), higher A1c (8.6 [2.2]%), and lower eGFR (52.7 [37.7] mL/min) (p&lt;0.001 for all) compared to those with T1DM but without TRD (n=738,984) After PSM, both T2DM and T1DM cohorts with TRD exhibited worse overall survival compared to their respective control groups (log-rank χ2=162.83, p&lt;0.001; log-rank χ2=13.56, p&lt;0.001).
Conclusion
Adults with T1DM and T2DM diagnosed with TRD face significantly higher mortality risk compared to those without TRD, despite adjusting for covariates. Key risk factors that may contribute to TRD development include Black race, hypertension, poor glycemic control, renal dysfunction, and lower socioeconomic status. These findings underscore the need for targeted management strategies to mitigate mortality risk in patients with diabetes and TRD. Future research should assess the effectiveness of interventions addressing TRD risk factors to improve survival outcomes in this high-risk population.

AMA Research Challenge 2025 

Risk Factors and Mortality Associated with Tractional Retinal Detachment in Type I and Type II Diabetes

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Background
Tractional retinal detachment (TRD) is a severe complication of diabetic retinopathy, but its risk factors and impact on mortality in patients with Type I (T1DM) and Type II (T2DM) diabetes remain underexplored. Given the rising prevalence of diabetes, understanding the key contributors to TRD development is critical. This study aims to identify risk factors for TRD and evaluate its effect on survival in individuals with T1DM and T2DM.
Methods
A retrospective study was conducted using the US TriNetX Network database, identifying adults with T1DM and T2DM who were diagnosed with TRD between 2010-2024. Baseline characteristics, including demographics, comorbidities, renal and glycemic labs, and use of antidiabetic medications, were collected within 1 year of diagnosis. Propensity score matching (PSM) of these characteristics was performed to compare T2DM patients with and without TRD, and the same analysis was repeated for T1DM patients. Data were expressed as n (%) or mean (standard deviation). The primary outcome was all-cause mortality over 10 years, analyzed with Kaplan-Meier curves and log-rank tests.
Results
Among 14,701 adults with TRD, 9,820 (66.8%) had T2DM and 3,903 (26.5%) had T1DM. Compared to T2DM patients without TRD (n=3,897,132), the T2DM and TRD cohort had a higher prevalence of Black race (3,172 [32.3%]), HTN (4,624 [47.1%]), adverse SDOH (176 [1.8%)]), higher A1c (8.4 [2.3]%), lower eGFR (53.0 [36.7] mL/min), and higher CRP (42.4 [68.2] mg/L) (p<0.001 for all). Similarly, the T1DM and TRD cohort exhibited higher prevalence of Black race (1,288 [33.0%]), smoking (68 [1.8%]), HTN (2,277 [58.4%]), adverse SDOH (108 [2.8%]), higher A1c (8.6 [2.2]%), and lower eGFR (52.7 [37.7] mL/min) (p<0.001 for all) compared to those with T1DM but without TRD (n=738,984) After PSM, both T2DM and T1DM cohorts with TRD exhibited worse overall survival compared to their respective control groups (log-rank χ2=162.83, p<0.001; log-rank χ2=13.56, p<0.001).
Conclusion
Adults with T1DM and T2DM diagnosed with TRD face significantly higher mortality risk compared to those without TRD, despite adjusting for covariates. Key risk factors that may contribute to TRD development include Black race, hypertension, poor glycemic control, renal dysfunction, and lower socioeconomic status. These findings underscore the need for targeted management strategies to mitigate mortality risk in patients with diabetes and TRD. Future research should assess the effectiveness of interventions addressing TRD risk factors to improve survival outcomes in this high-risk population.

poster

Background
Latent autoimmune diabetes in adults (LADA) is an underrecognized slowly progressive form of autoimmune diabetes that presents in adulthood and is frequently misdiagnosed as type 2 diabetes mellitus (T2DM) due to its indolent progression and overlap features of metabolic syndrome. Patients may initially respond to oral hypoglycemic agents but eventually require insulin therapy due to progressive beta-cell failure. Misdiagnosis can lead to suboptimal glycemic control and increased risk of complications, including DKA.
Case Presentation
A 60-year-old woman with asthma, hyperlipidemia, and type 2 diabetes was initially admitted to the ICU for euglycemic DKA. This occurred three weeks after a hospitalization for influenza. A–related respiratory failure. Labs in the ED revealed a high anion gap metabolic acidosis (gap 25, pH 7.2), blood glucose of 140 mg/dL, and moderate ketones, confirming euglycemic DKA. She was compliant with her medications, including empagliflozin/metformin, but was not on
insulin. Her HbA1c was 8.5%. From 2023–2025, she had eight diabetes-focused visits with consistent medication adherence. A prior GLP-1 trial was discontinued due to GI side effects. Despite nutrition counseling and lifestyle changes, her HbA1c remained between 8.5–9.3%. LADA was suspected and confirmed with positive ZnT8 antibodies. She was started on Lantus 10 units nightly and referred to
endocrinology. At follow-up, fasting glucose averaged 150 mg/dL—an improvement from baseline.
Discussion
In 2019, the WHO reclassified LADA as slowly evolving, immune-mediated diabetes in adults. It resembles adult-onset type 1 diabetes but presents with metabolic syndrome features, a single autoantibody (often GAD), and preserved β-cell function. LADA typically affects adults misdiagnosed with T2DM who test positive for pancreatic autoantibodies (GAD, IA-2, or ZnT8).
These patients initially manage without insulin but progress to insulin dependence faster than typical T2DM. The Immunology of Diabetes Society defines LADA by age ≥30, at least one positive diabetes-related autoantibody, and no insulin requirement within six months of diagnosis. C-peptide helps guide therapy: levels ≥0.7 nmol/L may allow for T2DM management, while < 0.3 nmol/L warrants full insulin therapy. SGLT-2 inhibitors, though cardioprotective in T2DM, pose a risk in LADA due to their association with euglycemic DKA. This is believed to result from increased glucagon, hepatic ketogenesis, and impaired ketone clearance. As β-cell function declines, the risk of DKA rises, similar to T1DM. Misdiagnosis of LADA as T2DM often delays appropriate treatment, increasing the likelihood of poor glycemic control and complications like DKA.

Unmasking Latent Autoimmune Diabetes: A case that challenges Type 2 Diabetes

Immune Thrombocytopenia in Pregnancy: Recognition, Risk, Response
Background
Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by isolated thrombocytopenia, which presents unique challenges in pregnancy due to potential bleeding risks and effects on the fetus. It occurs in 1 to 2 of every 1,000 pregnancies, which is a greater rate than in the general population. Thrombocytopenia in pregnancy can be connected to different etiologies, which can have very different consequences and are treated differently. ITP is a diagnosis of exclusion, so early recognition and close monitoring are essential to optimize maternal and neonatal outcomes.
Case Presentation
A 34-year-old G4P3 woman at 14 weeks gestation with a history of Hashimoto’s thyroiditis and gluten intolerance presented with mild fatigue and dyspnea on exertion. She was being evaluated for persistent thrombocytopenia during pregnancy, with laboratory studies revealing a platelet count of 104,000/μL with otherwise normal complete blood count and peripheral smear. She was also found to have iron deficiency without anemia. This was addressed with a trial of IV iron, resulting in improvement. Platelet counts during previous pregnancies, in chronological order, were 116k, 99k, and 92k. The patient denied any
bleeding issues and previous postpartum hemorrhages. Infectious and autoimmune panels were negative, and Von Willebrand disease was ruled out. There was no evidence of vitamin B12 or folate deficiency. A diagnosis of ITP was made based on exclusion and most likely given chronicity and personal medical history of other autoimmune disease processes. Besides closely watching the trend of her platelet count throughout her pregnancy, which stayed >100k and remained asymptomatic, no intervention was needed. Her platelet count was 125k 6 months postpartum.
Discussion
ITP in pregnancy requires careful distinction from gestational thrombocytopenia and more serious etiologies such as HELLP syndrome and preeclampsia. Treatment of ITP during pregnancy is generally the same as that outside of pregnancy and is focused on reducing the risk of bleeding rather than increasing platelet count. Platelet count should be checked at least every 4 weeks up until delivery. First-line therapy is indicated if the platelet count drops to <30k and includes corticosteroids with IVIG, with possible platelet transfusion. Decisions regarding delivery method and timing depend on platelet levels and maternal- fetal status. Platelet count requirements during delivery for the following procedures are: epidural >50-80k, c-section >50k, vaginal >30k. Neonate platelet count should be taken immediately after delivery to determine if therapy is needed. This case highlights the recognition and tailored therapy for ITP in pregnancy to ensure favorable outcomes.

Immune Thrombocytopenia in Pregnancy: Recognition, Risk, Response

Paget-Schroetter Syndrome is a form of upper extremity deep vein thrombosis that typically affects young, healthy individuals following repetitive arm movements or strenuous activity. It results from compression of the subclavian vein at the thoracic outlet, often due to anatomical abnormalities like a cervical rib or hypertrophied muscles. This compression can lead to vein injury and clot formation. Early diagnosis and treatment—including anticoagulation, possible thrombolysis, and surgical decompression—are important to prevent long-term complications.

A 39-year-old woman with a medical history of migraines and who uses a hormonal contraceptive vaginal ring presented to her physician with a swollen, discolored right arm. She reported right arm weakness for the past three months, and over the preceding week, she had noticed increased tightness in her sleeve along with numbness. Due to concern for deep vein thrombosis (DVT), point-of-care ultrasound (POCUS) was performed, revealing a thrombus in the subclavian and axillary veins. A formal ultrasound confirmed an occlusive thrombus in these veins, raising suspicion for Paget-Schroetter Syndrome. A CT scan of the chest was unremarkable. She started apixaban and referred to Interventional Radiology (IR). Venography performed by IR demonstrated high-grade stenosis of the distal subclavian vein at the level of the first rib, confirming the diagnosis. Successful angioplasty was performed. It was at that time that she was referred to vascular surgery. The patient ultimately underwent first rib resection and scalenus anticus resection to address a cervical rib contributing to the compression.

Tight Sleeves and Silent Stenosis: A Vascular Surprise

Clinical Implications of a Left Vertebral Artery Arising from the Aortic Arch
M. Culligan, D. Taneja, A. Charles, K. Thurmann, A. O’Neill, L. Suh, B. Wang, D. Taneja

Background: The left and right vertebral arteries typically originate as the first branches of the left and right subclavian arteries, respectively. Variations in their origin are fairly rare, with the left vertebral artery (LVA) arising as a fourth branch directly off the aortic arch in approximately 3.6-5.5% of the population. LVA abnormalities have the potential to complicate surgical and diagnostic procedures of the neck and surrounding vasculature. 

Case Presentation: During a cadaveric dissection of a 71-year-old female in the anatomy lab at Creighton University School of Medicine - Phoenix, the left vertebral artery was observed originating directly from the aortic arch, between the origins of the left common carotid artery and left subclavian artery. The LVA extended superiorly before entering the transverse foramen of the C5 vertebra. The LVA’s prevertebral length was 93.5mm, compared to 37.8mm for the right vertebral artery (RVA), which entered the spine at C6. The diameters at the base of the LVA and RVA were 2.7mm and 2.1mm, respectively. The brachiocephalic trunk and RVA branching from the right subclavian artery were anatomically unremarkable. Of note, an ependymal cyst in the left parietal lobe was discovered in a previous dissection of this cadaver, who was noted to have a history of epilepsy. 

Discussion: A LVA of aortic arch origin is classified as a Type III aortic arch abnormality. Type III LVAs tend to ascend medially and have a longer course prior to entering the transverse foramen of the vertebrae. This longer, and often more tortuous, prevertebral course can predispose patients to a greater risk of vertebral artery dissection, which presents with headaches and other neurological symptoms. The increased prevertebral, medially-running course also poses increased risk for complications such as hemorrhage, neurological deficits, and even death during anterior approach cervical spinal surgeries. Clinicians unaware of a LVA abnormality while attempting a carotid artery stent or aortic arch procedure could inadvertently occlude the LVA and cause cerebral ischemic effects. In catheterization and other diagnostic studies, a Type III LVA could be incorrectly considered occluded and subject to unnecessary treatment. Obtaining computed tomography angiography or magnetic resonance imaging studies to identify an abnormality prior to a procedure can prevent misdiagnosis and reduce the risk of vertebral artery damage and downstream complications. 


Clinical Implications of a Left Vertebral Artery Arising from the Aortic Arch

Background
Terminal extubation, or palliative or compassionate extubation, is a legally and ethically accepted practice in the US where mechanical ventilation is withdrawn when ongoing life-sustaining treatment no longer aligns with a patient’s goals of care, with nearly 42% of ICU deaths involving withdrawal of such measures. Despite its legal acceptance, it remains a nuanced decision, particularly in patients with spinal cord injury (SCI). Approximately 18,000 new SCIs occur annually in the US, with respiratory failure being the leading cause of death. While extubation protocols exist, there are none specific to the SCI population. Discussions around goals of care and prognosis for patients with SCI may be complicated by quality of life (QOL) concerns and potential ableist bias when physical dependence is misinterpreted as incompatible with meaningful life. Here, we present a case of an older adult with cervical SCI who requested terminal extubation following prolonged hospitalization.

Case Presentation
An 88-year-old male with a history of hypertension and prostate cancer sustained a traumatic high cervical SCI with craniocervical subluxation and multiple associated injuries. He required mechanical ventilation and underwent tracheostomy after developing respiratory failure and pneumonia, and his hospital course was further complicated by pneumonia, pressure injuries, and persistent ventilator dependence. Psychiatric evaluation initially raised concerns for depression and adjustment disorder, though he expressed a consistent, clear expression of a wish not to live ventilator-dependent. Over weeks across multiple care settings, he reaffirmed this wish. After comprehensive interdisciplinary assessment confirming decision-making capacity, and with strong family support, he elected for hospice care. Supported by his family and palliative care team, he was extubated and passed 48 hours later. 

Discussion
This case illustrates the complex intersection of autonomy, capacity, and ethics in end-of-life decisions for patients with SCI. Withdrawal of nonbeneficial life-sustaining treatment is ethically distinct from physician-assisted dying and aligns with guidelines from the American Academy of Hospice and Palliative Medicine, and the patient’s final decision was expressed consistently over time and across settings with concerns about mood disorders impairing decision-making carefully evaluated. SCI presents unique challenges to autonomy, especially when provider bias may influence care framing. QOL judgements must be patient-centered, informed by lived experience rather than assumptions. Physiatry plays a crucial role, offering prognostic insight and advocating for patient-centered goals. As terminal extubation becomes more common in ICU care, cases like this highlight the need for ethical, patient-centered approaches to end-of-life decision making.

Respecting Patient Autonomy in the Context of Terminal Extubation: A Case Report and Ethical Analysis

Introduction
Massive pulmonary embolism (PE) is a life-threatening condition that can present with cardiovascular collapse and cardiac arrest. Rapid recognition and timely intervention are crucial for improving patient outcomes. This case highlights a unique stepwise treatment approach, where systemic thrombolysis with tenecteplase (TNK) was initially administered, followed by catheter-directed thrombolysis (CDT) using the EkoSonic Endovascular System (EKOS), a strategy not commonly reported in the literature.
Case Presentation
A 69-year-old male with a history of class III obesity (BMI 43), untreated obstructive sleep apnea, non-insulin-dependent type II diabetes mellitus, and chronic lymphedema presented to the emergency department after a fall at a gas station. Emergency medical services (EMS) responded and found the patient severely short of breath. While being transported, he became unresponsive and was found to be in pulseless electrical activity (PEA) arrest, necessitating cardiopulmonary resuscitation (CPR). Return of spontaneous circulation (ROSC) was achieved before intubation, and the patient arrived at the emergency department with tachycardia, hypotension, and oxygen saturation of 96% on a non-rebreather mask.
Given the hemodynamic instability and history of sudden cardiovascular collapse, an emergent computed tomography (CT) angiogram of the chest was performed, revealing bilateral massive pulmonary emboli with right heart strain. Two rib fractures, likely secondary to CPR, were also noted. A transthoracic echocardiogram demonstrated a normal ejection fraction (55%) with a moderately enlarged right ventricle, McConnell’s sign, and moderate-to-severe tricuspid regurgitation consistent with right heart strain. A diagnosis of acute bilateral PE with cor pulmonale was made..
Given the patient’s unstable hemodynamics and contraindications to full-dose thrombolysis, cardiology was consulted for EKOS catheter-directed thrombolysis. However, at that time, he was deemed unsuitable for the procedure. Instead, he received half-dose systemic TNK (50 mg) due to concerns over his rib fractures. He was started on intravenous heparin and admitted to the intensive care unit for close monitoring.
Despite initial improvement in oxygenation, the patient developed worsening hypotension requiring increasing doses of norepinephrine. Due to persistent hemodynamic instability, the decision was made to proceed with EKOS catheter-directed thrombolysis. The catheter was placed for direct administration of tissue plasminogen activator (tPA) into both pulmonary arteries. The patient tolerated the procedure well, with subsequent hemodynamic stabilization and improved blood pressures. He was transitioned from heparin to apixaban and vasopressor support was weaned. Patient was discharged home shortly after in stable condition.
Discussion
This case underscores the effectiveness of EKOS catheter-directed thrombolysis in treating massive PE, particularly in patients with contraindications to full-dose systemic thrombolysis. While TNK served as an initial bridge to slow clot progression, hemodynamic deterioration necessitated escalation to EKOS, which successfully facilitated clot resolution. The use of ultrasound-assisted CDT offers the advantage of lower thrombolytic doses with enhanced clot penetration, reducing the risk of bleeding while achieving rapid hemodynamic stabilization. This case highlights the importance of considering EKOS as a definitive intervention in high-risk PE cases, particularly when systemic thrombolysis alone proves insufficient.
This case underscores a novel treatment approach combining systemic TNK followed by EKOS-directed CDT in a patient with massive PE. This strategy may offer a balanced approach in select patients, allowing for initial clot lysis with reduced bleeding risk while preserving the option for targeted intervention. Multidisciplinary collaboration remains essential in optimizing outcomes for this high-risk population.


Sequential Thrombolysis with Tenecteplase Followed by EKOS in Massive Pulmonary
Embolism

Abstract Title: A Cross-Rank Analysis of Gender Disparities in Promotional Salary Scaling in Academic Medicine

Background
Gender-based disparities remain persistent and widespread throughout academic medicine. Recent studies show that women are less likely to be promoted from assistant to associate professor, from associate to full professor, and to department chair. Women also receive unequal compensation in nearly all specialties, with differences primarily originating from lower starting salaries. Though the differences in advancement and salary have been examined prior, there is 
still more to learn about the differences in promotional salary scaling – that is, the relative increase in salary with advancement in academic rank – between genders. This study investigates that comparison.

Methods
We analyzed gender-based differences in salary increases using data from the AAMC 2023 Fiscal Year Report, which includes summary statistics (mean, SD, and count) on total compensation for MD or equivalent faculty. Salary data were analyzed across academic ranks from instructor to chair in both “Total Medicine” and “Total Surgery.” Z-statistics were used to compare differences in promotional salary increases between male and female faculty. To estimate average percent 
change differences and 95% confidence intervals, we conducted 10,000 parametric bootstrap simulations using the reported summary data at each promotion level. All z-tests were two-sided with significance set at p<0.05.

Results
After conducting the simulations in Total Medicine, between instructor to assistant professor (n=13,358) men received an average raise $30,952 higher than women (95% CI: $19,844–$42,060; p<0.001). There was also a mean difference of $10,160 (95% CI: $1,735–$18,585; p=0.018) from assistant to associate professor (n=17,410). Simulated percent change in salary from instructor to assistant professor showed a 10.5% advantage for men (95% CI: 4.95–16.49%). In Total Surgery, there were also higher raises on average for men compared to women. From assistant to associate professor (n=6,833), the difference was $29,332 (95% CI: $3,708–$54,957; p=0.025). From professor to chief (n=2,874), it was $89,462 (95% CI: $5,308–$173,616; p=0.038). However, when looking at the simulated percent changes in salary, there was no statistically significant change between genders at any promotional level. 

Conclusion
While no consistent disparities in promotional salary scaling were observed across all ranks or specialties, a significant gender-based difference in relative salary increase was identified at the instructor-to-assistant professor level in medical subspecialities. This early-career inequity may 
contribute to long-term salary divergence, which is well-documented. These findings also highlight the need to examine how initial promotion practices shape broader patterns of compensation inequality in academic medicine.

A Cross-Rank Analysis of Gender Disparities in Promotional Salary Scaling in Academic Medicine​

Background
While caregiving burden with dementia diagnoses has been extensively documented, limited research has examined spousal and adult-child differences with dementia caregiver burden. This scoping review aimed to: (1) synthesize differences in dementia caregiver burden between spouse and adult-child dementia caregivers, and (2) determine whether there was relationship status group that consistently experienced more caregiver burden.

Methods
A literature search was conducted on October 16th, 2024, using PubMed, Ovid, and Scopus. Included studies (published in English between January 1991 and June 2024) examined: (1) the impacts of caregiving for an individual with any form of dementia; (2) kinship distribution of study population and/or stratified results based on relationship status (spouse versus adult-child); and (3) caregiver burden as a unique, separate variable. Studies were excluded if: (1) described a psychological or physical disability that requires caregiving without a formal dementia diagnosis; (2) included formal and informal caregivers not stratified by kinship; and (3) examined a caregiver tool as a moderator of caregiver burden.

Results
A total of fifteen studies (out of 173 possible studies) met the scoping review criteria and were divided into quantitative (N=14) and qualitative interview (N=1) studies. Of the fifteen studies, six studies found that adult-children caregivers experienced more caregiver burden than spousal caregivers. Findings that showed spouses experienced more caregiver burden than adult-children were shown in four studies with only one of these studies reporting this difference at a medium effect size. Additionally, one study that stratified adult-children by live-in status, showed that adult-children who lived with the dementia patient reported the most burden followed by spouses and finally adult-children who did not live with the dementia patient experienced the least burden. The remaining three quantitative studies did not observe a difference in total caregiving burden with dementia patients between adult-children and spousal caregivers. Lastly, the one qualitative interview study found profound differences in the types of burden experienced by caregivers depending on their relationship to the dementia patient as psychological processing of the disease can change by position in the familial life cycle.

Conclusion
Overall, caregiver burden is significant and varies by caregiver relationship. Results were mixed regarding which group consistently experiences greater burden. Future longitudinal and cross-cultural investigations should further examine these associations within the dementia caregiving space, especially given an increasingly interconnected and aging world.

A scoping review of spouse and adult-child dementia caregiver burden: Who bears the brunt of the burden?

Background/Objectives: Perinatal asphyxia significantly threatens newborns, particularly in regions with limited maternal-fetal care. Neonatal hypoxic-ischemic encephalopathy (HIE), a consequence of perinatal asphyxia, can cause severe neurological damage if untreated. Therapeutic hypothermia is an effective intervention for HIE, demonstrated by the Brain Rescue of Infant with Graded Hypothermia Therapy (BRIGHT) program in Kampala, Uganda. However, this treatment remains inaccessible in many other regions of Uganda. This study assessed healthcare providers’ knowledge, attitudes, and practices (KAP) regarding birth asphyxia management and therapeutic hypothermia in the rural district of Kisoro and the urban district of Gulu.

Methods: A KAP survey was administered to 200 healthcare providers (75 in Kisoro, 125 in Gulu) from June to August 2024. Data included knowledge, attitudes, and practices regarding neonatal care, alongside demographics. Providers under 18 or non-English speaking were excluded. Composite scores for major concepts were calculated. SPSS v.29 was used for data analysis, including descriptive statistics, independent t-tests to compare responses between Kisoro and Gulu, and Pearson’s r correlations to explore relationships.

Results: While most participants demonstrated high knowledge of birth asphyxia (mean scores: 13.15 Kisoro, 13.06 Gulu; p < .001), gaps in therapeutic hypothermia knowledge persisted. Providers showed willingness to improve HIE management (mean scores: 12.99 Kisoro, 12.42 Gulu; p < .001). However, fatalistic beliefs potentially hindered interventions (mean scores: 5.20 Kisoro, 4.97 Gulu; p < .001). Reports of barriers to care were found to be more significant in Kisoro, with providers expressing concerns about therapeutic hypothermia feasibility (mean scores: 3.60 Kisoro, 3.08 Gulu; p = 0.041).

Conclusions: Knowledge gaps, resource limitations, and fatalistic beliefs challenge therapeutic hypothermia implementation, with barriers more pronounced in rural Kisoro. Addressing these through targeted training and resource improvements is critical to enhancing neonatal care in Uganda.

KABP Survey on Therapeutic Hypothermia for Perinatal Asphyxia among Healthcare Professionals in the Kisoro and Gulu districts of Uganda

Background
Methanol is a highly toxic, colorless, volatile alcohol that is present in homemade beverages, paint removers, windshield liquid, anti-freeze, shellac, and perfumes. Although uncommon in the United States, methanol poisoning can occur with improper distillation of spirits. Over 50% of morbidity and mortality associated with methanol poisoning is accidental in nature and therefore preventable. Methanol poisoning, even in small quantities of 50 to 100 ml, is associated with severe complications such as permanent blindness.
Aim
The aim of this study was to elaborate on a case of methanol poisoning and provide a deeper understanding of bilateral basal ganglia hemorrhage, which is a relatively rare complication of methanol ingestion.
Case report
A 28-year-old Caucasian female with a history of seizures was brought to the emergency department after being found unresponsive due to ingestion of hand sanitizer and mouthwash. Due to severe hypoventilation and concern that the patient would not be able to protect her own airway, she was intubated. Physical examination revealed that the patient was cyanotic with dilated and sluggish pupils. Blood work was remarkable for a low bicarbonate, transaminitis with an aspartate transaminase to alanine transferase ratio of 2:1, and an elevated anion gap. Arterial blood gas revealed lactic acidosis and metabolic acidosis. The osmolar gap was elevated. Serum ethanol and acetaminophen levels were negative. A head CT scan showed bilateral basal ganglia hemorrhage with surrounding edema. The volatile alcohol screen was positive for methanol. The patient was started on fomepizole. Unfortunately, she passed away the following day.
Discussion
Methanol is lethal when ingested above 1 g/kg of body weight. Clinical manifestations of methanol intoxication typically present 12 to 24 hours following the ingestion of methanol. Methanol is converted to formic acid, a toxic metabolite, by alcohol dehydrogenase in the liver. The early clinical features of methanol poisoning include headache, vomiting, weakness, and abdominal pain. After 24 hours of ingestion, formic acid causes end-organ damage to the retina, optic nerve, and basal ganglia. Visual manifestations include optic disc hyperemia, edema, central scotoma, and permanent blindness. This is a result of optic nerve atrophy and demyelination, which occur due to the inhibitory effect of formic acid on mitochondrial ATP production and anoxia. Neurological manifestations include seizures, coma, and death secondary to ischemic necrosis or hemorrhagic injury to the basal ganglia, especially the putamen and subcortical region. The exact etiology of necrosis and hemorrhage of the basal ganglia secondary to methanol poisoning remains unknown. However, it is thought to be secondary to the direct toxic effect of methanol and its metabolite formic acid. The management of methanol toxicity includes preventing further formic acid production by inhibiting alcohol dehydrogenase using either fomepizole or ethanol. It also includes the removal of previously accumulated methanol and formic acid from the blood with the correction of metabolic acidosis by hemodialysis and sodium bicarbonate infusion. This case report emphasizes the importance of early detection of methanol poisoning to prevent overt fatal outcomes.

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