Hospital medicine providers who responded to the survey reported encountering delirium often in their clinical practice; however, they also reported poor familiarity with and demonstrated poor knowledge of the CAM. These results suggest a potential barrier to systematic inpatient delirium screening and support increased delirium education and the use of validated delirium assessments among hospitalists.
Background Calciphylaxis is a rare, often fatal disease resulting from calcification of dermal arterioles and capillaries. Usually diagnosed in patients with end-stage renal disease, this disorder typically presents as necrotic, nonhealing ulcers in acral or adipose areas. Here we report the case of an elderly man who was found to have calciphylaxis of the distal digits and penis, the latter of which is an uncommon site of disease that carries a particularly poor prognosis. Case presentation A 73-year-old African American man with multiple medical comorbidities including dialysis-dependent end-stage renal disease presented with worsening painful, necrotic lesions on his glans penis and several distal digits over the last 2 months. The wound on the glans was foul smelling with overlying purulence and had been unsuccessfully treated with amoxicillin–clavulanic acid. Discovery of diffuse intravascular calcification on computed tomography, in addition to a markedly elevated calcium–phosphate product immediately prior to the onset of his ulcers, led to the diagnosis of calciphylaxis. The patient was initiated on sodium thiosulfate without improvement in his lesions, and he died 3 months later after another prolonged hospitalization. Conclusions While calciphylaxis is a rare disease, involvement of the distal digits and especially the penis is even more uncommon and portends a particularly poor prognosis: 6-month mortality rates are reportedly as high as 70%. This suggests that prompt recognition and management of the disease is required; however, despite receiving standard therapy, our patient failed to experience improvement in his disease and instead developed several more fingertip ulcers at blood glucose sample points during his hospitalization. A corollary of the case presented here is the need for more effective management of calciphylaxis, especially for patients in whom uncommon sites, such as the penis, are involved.
An 80-year-old man with a history of hypertension, gastroesophageal reflux disease, and stage 4 chronic kidney disease presented with 2 days of anuria. He felt well until 6 days prior, when he awoke with diffuse muscle cramps following a strenuous day of moving boxes. He subsequently developed oliguria that progressed to anuria. His only medication was omeprazole (20 mg daily). His usual fluid intake had not changed.Physical examination was notable for moist mucous membranes, clear lungs, no lower extremity or periorbital edema, and no jugular venous distension. Examination was otherwise unremarkable. Bladder scan showed 50 mL of urine, which was collected via straight catheterization. Three liters of normal saline was administered, with no further urine production.Laboratory testing revealed a blood urea nitrogen level of 90 mg/dL (32.1 mmol/L) (reference range, 7-21 mg/dL [2.5-7.5 mmol/L]) and creatinine level of 14.1 mg/dL (1246.4 μmol/L) (reference range, 0.6-1.17 mg/dL [53.0-103.4 μmol/L]); baseline levels 3 months prior were 37 mg/dL (13.2 mmol/L) and 3.3 mg/dL (291.7 μmol/L), respectively. Hemoglobin level was 10.6 g/dL (reference range, 13-17 g/dL); calcium, 8.1 mg/dL (reference range, 8.5-10.1 mg/dL); potassium, 6.2 mmol/L (reference range, 3.5-4.7 mmol/L); and phosphorous 8.8 mg/dL (2.8 mmol/L) (reference range, 2.5-4.9 mg/dL [0.81-1.58 mmol/L]). Creatine kinase level was within normal limits. Urinalysis showed minimal albuminuria (100 mg/dL); however, spot urine protein to creatinine ratio predicted 11 139 mg/g (reference range, 0-200 mg/g) proteinuria. Renal ultrasound showed no hydronephrosis. Serum protein electrophoresis and immunofixation electrophoresis identified a small monoclonal IgG κ band. Serum κ free light chain (FLC) level was 20 765 mg/L (reference range, 3.3-19.4 mg/L) with a free κ to λ ratio of 296 (reference range, 0.37-3.1). 1 Hemodialysis was initiated and a bone marrow biopsy obtained.Bone marrow biopsy showed a normocellular bone marrow with 10% κ-restricted plasma cells (Figure , left panel). Immunohistochemical staining demonstrated positivity for the plasma cell marker CD138 (Figure, right panel).Figure. Left, Bone marrow biopsy sample (hematoxylin-eosin, original magnification ×400). Right, Immunohistochemical staining of biopsy sample (immunohistochemical stain for CD138, original magnification ×400).
Background: The practice of race-based medicine fails to recognize that race cannot be used as a proxy for genetic ancestry and that racial and ethnic categories are complex sociopolitical constructs without biological basis. Clinical algorithms and equations that incorporate race modifiers and are currently considered standard for diagnosis and management of disease are appropriately being scrutinized for lack of biological plausibility and their role in exacerbating health inequities. In this paper, we review the history, evidence, and implications of using a Black race coefficient when calculating estimated glomerular filtration rate (eGFR) in the diagnosis and management of kidney disease. Observations: Currently, the US Department of Veterans Affairs (VA) uses the Modification of Diet in Renal Disease (MDRD) equation for eGFR. This equation includes a Black race coefficient that results in an eGFR that is 21% higher for a Black patient when compared with a patient of any other race. The rationale for the inclusion of this coefficient is based on racist science that incorrectly assumes race as a proxy for genetic ancestry. Multiple studies across diverse Black populations demonstrate that the application of a race coefficient in kidney function estimation equations is inferior when compared with the race-neutral option. Furthermore, the most utilized eGFR equations are biased and imprecise. Because eGFR is the primary diagnostic method for detecting and managing kidney disease, preventing its progression, planning for dialysis, and evaluating for transplantation, it is vital that eGFR be as accurate, precise, and equitable as possible. Conclusions: The incorporation of a race coefficient in kidney estimation equations lacks biological plausibility and its use exacerbates kidney health disparities. Until a better method to estimate kidney function becomes available, a race-neutral option for current estimation equations should be applied for all patients.
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