Journal of Community Hospital Internal Medicine Perspectives最新文献

We present the case of a young man in his early thirties who sought medical attention after a witnessed seizure episode. His drug screen revealed the presence of cocaine, marijuana, and benzodiazepines. To investigate any potential structural causes contributing to his seizure, we conducted an MRI of the brain, which revealed polymicrogyria. This structural abnormality is strongly associated with seizures. This case emphasizes the importance of ruling out underlying structural causes of seizure disorders in patients with a history of drug abuse before recommending cessation of drug use.

Pasteurella multocida is a non-spore forming gram-negative organism characterized morphologically as coccobacillus. It is frequently isolated from the nasopharynx of domestic and wild animals, and is the most common cause of soft-tissue infection in humans following bites or scratches from dogs and cats. It is easily overgrowth by other flora in the sputum and may be regularly overlook, as it resembles Haemophilus influenzae, Francisella tularensis, and Yersinia pestis. The five species that cause the majority of pasteurellosis are: multocida, septica, canis, stomatis, and dagmatis. Pasteurella multocida is infrequently encounter in clinical settings, although it can cause disease in humans primarily through contact with animals or their mucous secretions. Furthermore, Pasteurella multocida serves as an opportunistic pathogen in humans, especially in those with depressed immune system. In this report, and after extensive literature review, the authors described a patient with septic shock resulting from Pasteurella multocida bacteremia without prior history of animal exposure.

Acute esophageal necrosis (AEN) is a rare syndrome, characterized by extensive circumferential necrosis of the esophageal mucosa at the gastroesophageal junction. AEN carries significant morbidity and mortality, and early recognition is crucial for management. We present a case series of AEN in two critically ill patients, one who presented with coffee ground emesis and diabetic ketoacidosis (DKA) and the other one who presented with upper gastrointestinal bleed in the setting of malignancy and concurrent infection with active antibiotic use. Prompt diagnosis and management of both AEN and its underlying causes are crucial to improve patient outcomes.

Background: Leukemia ranks among the top three cancers in those who have Acute Kidney Injury (AKI), with an incidence of 7.5 % in hematological malignancies. Through this study, we aimed to assess the mortality of severe sepsis (SS), thrombocytopenia, and metabolic encephalopathy (MetE) in Leukemia with AKI.

Methods: We conducted a retrospective analysis using the National Inpatient Sample (2018-2021). Adults with Leukemia primarily admitted with AKI were included, and mortality was calculated. Patients were stratified by SS, thrombocytopenia, and MetE. Propensity matching for age over 60 and gender, and multivariate regression were performed with p ≤ 0.05.

Results: Among 388,449 Leukemia patients, 2.5 % had AKI. The mortality in AML was 7 % and CML was 5.7 %. In Leukemia, mortality risk was lower in the AKI cohort than in those without AKI (aOR 0.04, p < 0.01). In the AKI cohort, individuals aged >60 years showed increased mortality (p < 0.001). Race, gender, hematopoietic stem cell transplant, and inpatient hemodialysis did not alter mortality (p > 0.05). We identified increased mortality risk with SS (aOR 38.2, p < 0.001), thrombocytopenia (aOR 1.8, p < 0.001), and MetE (aOR 3.3, p < 0.001). Additionally, patients with these outcomes required blood transfusions, vasopressors, and invasive ventilation (p < 0.001).

Conclusion: These findings underscore the lower mortality of AKI in Leukemia but highlight higher mortality rates in association with sepsis, thrombocytopenia, and metabolic encephalopathy. Managing AKI also requires appropriate antibiotic selection and a thorough evaluation for bone marrow dysfunction.

Drug-induced antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a condition caused by a few culprit medications, notably hydralazine. Despite the significant morbidity and mortality associated with this condition, its rarity makes timely diagnosis challenging. A 68 year-old female presented to her nephrologist for a routine follow up of her chronic kidney disease stage III secondary to hypertension. Routine lab work noted worsened creatinine and protein to creatinine ratios. Additionally, her hypertension became more difficult to control, and she suffered from malaise, poor appetite, joint aches/pains and lower extremity edema. Given her sudden worsening of renal function, a serologic investigation was performed which revealed an elevated ANA, dsDNA, and anti-PR3. Renal biopsy showed a membranous pattern of immune-complex glomerulonephritis, necrotizing crescentic lesions, and focal acute tubular injury, concerning for SLE membranous nephropathy and overlapping AAV. She was diagnosed with both SLE and AAV and began empiric treatment with prednisone and rituximab as well as hydroxychloroquine. Several months later a medication review noted over 10 years of hydralazine use, with doses up to 125 mg twice daily. Given her presentation, biopsy, auto-antibodies, and hydralazine use, hydralazine-induced AAV was considered, and the medication was discontinued. She was eventually transitioned to mycophenolate and was deemed in remission. However, two years later her disease flared, and she passed away from diffuse alveolar hemorrhage related to AAV. This case illustrates a rare adverse effect of a commonly used medication. Awareness of this disorder is essential in guiding discontinuation of the drug and obtaining appropriate treatment.

Mycoplasma pneumoniae pneumonia (MPP) most commonly presents as bronchitis or as a self-limited 'walking' community acquired pneumonia. A fulminant form of MPP may occur in 0.5 %-2 % of patients and is characterized by rapidly progressive respiratory failure and Acute respiratory distress syndrome (ARDS). Our case highlights the importance of considering fulminant MPP as a cause of ARDS, especially in the young adult and middle-aged population. We review the current literature and management principles of this rare disease with an emphasis on antibiotic stewardship and corticosteroid therapy. Further research is needed to better understand patterns of antibiotic resistance and to establish management guidelines for fulminant MPP.

Acute generalized exanthematous pustulosis is an uncommon cause of rash, typically presenting with pustules with an erythematous base and associated skin-peeling. Frequently caused by medications, including penicillins and quinolones, cephalosporins are rarely reported as an offending agent. Here, we present a case of rare acute generalized exanthematous pustulosis secondary to recent cephalosporin use presenting to our rural healthcare facility. We aim to raise awareness of this unusual rash secondary to cephalosporin use.

Necrotizing Fasciitis (NF) is a severe, potentially fatal soft tissue infection leading to death of muscles, fascia, and surrounding tissue. Perforated colon cancer (CC) is an exceedingly uncommon cause of NF. Here, we present a case of NF secondary to perforated colon cancer. This case emphasizes the significance of prompt identification, aggressive surgical excision of affected tissue, and consideration of rare, yet potentially fatal underlying etiologies in the management of NF as well as underscores the importance of CC screening to prevent devastating complications and mortality.

Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease characterized by the presence of circulating autoantibodies. The spectrum of disease manifestations extends from asymptomatic cases to mild symptoms and, in rare instances, acute liver failure. AIH is a diagnosis of exclusion, supported by the detection of autoantibodies such as anti-smooth muscle antibody (ASMA). This case describes a 43-year-old female with myasthenia gravis, receiving monthly intravenous immunoglobulin (IVIG) infusions, who presented with persistently elevated liver enzymes and mildly elevated ASMA titers across multiple clinical encounters. A liver biopsy revealed severe acute hepatitis. While drug-induced liver injury (DILI) secondary to IVIG was initially considered the leading diagnosis, the persistence of elevated liver enzymes over two months despite discontinuation of IVIG made the diagnosis of AIH more likely and brought attention to the diagnostic challenges associated with AIH. Although ASMA is a hallmark serologic marker for AIH, it only has a moderate sensitivity of 59 %. Furthermore, IVIG administration may interfere with autoimmune testing, potentially leading to false-negative results. This case illustrates the complexity of interpreting autoimmune serologies and emphasizes the need for comprehensive diagnostic approach. It also highlights the importance of recognizing cognitive biases, such as premature diagnostic closure, that can hinder accurate diagnosis.

Background: Atherosclerosis, a major cause of cardiovascular morbidity and mortality, involves lipid accumulation, endothelial dysfunction, inflammation, and oxidative stress. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, initially developed for type 2 diabetes mellitus (T2DM), have demonstrated cardiovascular benefits beyond glycemic control. Emerging evidence suggests their potential role in slowing atherosclerosis progression and enhancing plaque stability.

Methods: A systematic review of PubMed, Scopus, Embase, and Cochrane Library databases was conducted to identify preclinical and clinical studies on SGLT2 inhibitors and atherosclerosis. Studies published in English up to December 2024 were screened using predefined criteria. Data on mechanisms, lipid metabolism, endothelial function, vascular inflammation, and plaque stability were extracted, and study quality was assessed.

Results: A total of 16 animal and 4 human studies were included. SGLT2 inhibitors (empagliflozin, dapagliflozin, and canagliflozin) improved glycemic control, lipid metabolism, and atheroma reduction while enhancing plaque stability. They modestly reduced triglycerides and LDL-C while increasing HDL-C. SGLT2 inhibitors also decreased vascular inflammation and enhanced plaque stability by increasing fibrous cap thickness. Cardiovascular outcome trials demonstrated reductions in major adverse cardiovascular events (MACE) and heart failure hospitalizations, indirectly supporting their atheroprotective role.

Conclusion: SGLT2 inhibitors offer a multifaceted approach to atherosclerosis management by improving lipid metabolism, endothelial function, vascular inflammation, and plaque stability. While evidence is promising, further research is needed to confirm direct anti-atherosclerotic effects, optimize their role in cardiovascular care.