Montgomery General Hospital

Metformin is a widely prescribed medication for the management of type 2 diabetes. It is known to have a high safety index; however, it can cause serious adverse effects such as lactic acidosis, particularly in patients with chronic kidney disease. Elderly patients are at higher risk of developing metformin-associated lactic acidosis (MALA) due to aging kidneys. We present an 82-year-old male with a past medical history of diabetes, stage 2 chronic kidney disease, atrial fibrillation on apixaban, stroke, and chronic stage 4 sacral decubitus ulcer who was sent to the emergency department (ED) for altered mental status. He was admitted to the intensive care unit for the management of septic shock, pulseless electrical activity (PEA) cardiac arrest, and acute hypoxemic respiratory failure requiring intubation. Laboratory tests showed lactic acidosis and anion gap metabolic acidosis in the absence of an infectious source. The patient had chronic kidney disease with acute renal failure on metformin. He was diagnosed with MALA. This case highlights the potential risks associated with metformin use in older adults with chronic kidney diseaseand acute kidney injury from infections, dehydration, and decreasing oral intake due to acute illness, aging, or dementia. There are expected physiological changes in the aging kidney, including cellular dysfunction and nephrosclerosis, that can cause unexpected kidney injury in older adults, causing their estimated glomerular filtration rate (eGFR) to drop acutely. Age-related changes in renal function and decreased clearance of drugs place elderly patients at higher risk of developing MALA. Guidelines for reducing or deprescribing metformin can be considered in older adults. This could prevent morbidity, mortality, and adverse outcomes in frail older adults with diabetes.

Intensive care units (ICU’s) are particularly susceptible to resource and personnel strain given the complexity and unpredictability of care. This featured prominently in the early course of the SARS-CoV-2 (COVID-19) pandemic, where poor patient outcomes were clearly linked to the increasing severity of ICU strain associated with decreased ICU capacity. Despite attempts at measuring ICU strain, there exists no operational model that ICU directors can implement to monitor strain or researchers can use to examine its effects. This article reviews ICU strain indicators including census load (census, acuity, and admissions), ICU flow characteristics (admission/discharge criteria, sufficient staffing levels, and ICU performance), and consequence mediators (ICU queuing time and high-risk discharges) with attention to common themes and measures. Census load data suggests mortality risk is greater when ICU census starts higher, has high overall acuity, and with greater numbers of admissions especially when they arrive close together. Optimal ICU flow depends on maintaining a “strain mindset” when prioritizing patients, optimal ICU professional staffing, and maintaining high level ICU performance processes. Finally, delaying ICU admissions beyond six hours, or “after hours” or rushed ICU discharges result in increased mortality risk. Incorporating these ICU strain factors into an outcomes-focused model is proposed based on a conceptual framework with future research objectives recommended.

Social determinants of health are rooted in structural racism. The healthcare community has long recognized the existence of significant race- and ethnicity-related health disparities. Yet pervasive disparities persist despite ongoing calls for institutions and healthcare professionals to promote health equity by addressing bias, discrimination, and social determinants of health. All PAs must take responsibility for the various ways in which we may unwittingly reinforce racism in our profession, and must shift our focus from treating the effects of racism to preventing them.

Nineteen thirty-eight was the last full season played by baseball slugger Lou Gehrig before amyotrophic lateral sclerosis (ALS) forced him to retire. He struggled to hit and field well for much of the season, and his final statistics -- a .295 batting average, 29 home runs, 114 runs batted in – were unusually low for him. But in mid-season, Gehrig enjoyed a streak in which he seemed to regain his previous power. This three-week stretch, not studied closely by neurologists or baseball historians until now, suggests that the “Iron Horse” may have experienced a temporary ALS reversal, which can be instructive for researchers and those coping with the disease.

geriatrics service line administrator, MedStar Montgomery Medical Center, Olney, Maryland The author declares no conflicts of interest.

Case Presentation: An 89-year-old woman with a history of atrial fibrillation, coronary artery disease, hypertension, and recent hospitalization for intraparenchymal and intraventricular hemorrhage presented with new-onset critical thrombocytopenia secondary to amiodarone, which had started approximately 1.5 months prior to presentation. Discussion: The patient’s treatment with amiodarone was stopped on the first day of admission, at which time her platelet count was 8x109/L. She received transfusions of 4 units of platelets during her hospital stay, and her platelet count was 41x109/L at discharge. It increased to 71x109/L at follow-up with outpatient hematology 15 days after presentation and was within normal limits 7 months after hospitalization. There are 2 published reports detailing 5 separate cases of amiodarone-induced immune thrombocytopenia, and at least 8 reports of amiodarone-induced bone marrow granulomas resulting in pancytopenia. Because the patient did not have pancytopenia consistent with myelosuppression, her presentation was not reflective of bone marrow granulomas or a direct, nonimmune-mediated insult. However, the return of her platelet count to a normal level was delayed compared with the timeline presented in previous cases of both amiodarone and non-amiodarone immune-mediated thrombocytopenias. This delay in return to normal platelet count was likely secondary to the patient’s older age in the context of amiodarone’s lipophilic nature and very long half-life. Conclusion: Although a rare complication of amiodarone use, thrombocytopenia should be considered by physicians who prescribe this drug. Signs of thrombocytopenia in the context of newly prescribed amiodarone should prompt a complete blood count, discontinuation of the drug, and monitoring for resolution. If the platelet count recovers and amiodarone is found to be responsible, the medication should not be restarted, and amiodarone should be considered a drug allergy.

Dexmedetomidine (dex) is an alpha 2A adrenergic receptor agonist that is used clinically as a sedative. Dex is thought to induce sedation via disinhibition of the preoptic area which is similar to what occurs during non-rapid eye movement (NREM) sleep induction. Human, cat and rat electroencephalogram (EEG) studies have shown similarities between NREM sleep and dex induced sedation in delta power and spindle activity. We tested the hypothesis that dex induces changes in the EEG that are similar to natural NREM sleep in young adult and old B6 mice. Male B6 mice aged 4-5 months (young adult) and 10-18 months (old) were implanted for EEG/EMG recording from prefrontal cortex, parietal cortex and cerebellum. Seven days after the surgery mice received intraperitoneal saline (vehicle) or dex (50, 100, 200, 400 mug/kg) injections and electrophysiology was recorded for at least 4 hours. Wake, NREM, REM and sedation were visually scored. Spectral differences between dex sedation and NREM sleep were analyzed using Fourier based multitaper methods. Dex induced dose dependent sedation and suppression of REM sleep in both young adult and old mice. Dex sedation produced from higher doses contained increased delta power for the first ~90 minutes followed by attenuation of frequencies above 10 Hz compared to NREM sleep. Immediately following dex administration, high voltage spike waves were observed in the prefrontal cortex EEG for the first 10-15 minutes. High voltage spikes had a fundamental frequency of 3-3.5 Hz and were narrow with sharp peaks resembling epileptiform activity. Old mice had significantly more spikes than young adults. These data support the idea that dex induces a sedated state that is distinct from NREM sleep. The elderly or people prone to seizures may have increased spike activity when given dex. none