Abstract Literature suggests racial implicit bias can significantly affect quality of care. Data demonstrates that older adult Blacks are twice as likely to have dementia as their White counterpart. Inappropriate cognitive screening by providers or diagnosing dementia just based on clinical impression could easily result in an over or under-estimation of the dementia. We reviewed the rate and method of cognitive screening in randomly selected patient records (n=75) at a primary care university clinic. Our results indicated that the cognitive screening rate for Black patients was lower compared to their White counterpart (43.4% Blacks vs 68.5% Whites, p < 0.05). We designed a quality improvement project to identify any contributory causes and challenges involved in screening for dementia with the goal to reduce racial disparity in dementia diagnosis. We identified knowledge deficits in providers in their approach towards patients with dementia and a lack of experience in their use of appropriate instruments for cognitive screening. A multipronged educational program, with videos, case conferences, presentations and one-to-one training by dementia experts and a neuropsychologist was employed to reduce the bias and train the providers in appropriate screening methods. Post-educational intervention, screening rates greatly improved in n=75 randomly selected patients from both races. In Whites, the screening rate increased by 20.9% to 89.4% and in Blacks by 38.9% to 82.3% (p < 0.05). Overall, the quality improvement driven educational intervention improved the self-efficacy of providers and improved the standardized dementia screening rates in Black patients to levels comparable to those of White patients.

Introduction: Hypercalcemia is relatively common in clinical practice. Primary hyperparathyroidism and malignancy accounts for more than 90 percent of all cases of hypercalcemia. Milk alkali syndrome which is hypercalcemia classically caused by ingestion of large amount of calcium and absorbable alkali which was once virtually disappeared as a cause of hypercalcemia has emerged as a third leading cause of hypercalcemia. We present a case of hypercalcemia secondary to ingestion of calcium carbonate tablets resulting in milk alkali syndrome.Case presentation: Patient is a 45-year-old female with history of gastroesophageal reflux disease came to the emergency department with complaints of dizziness, constipation, fatigue and confusion for 3 weeks. She was hypotensive to 83/53 mmHg at arrival. Significant laboratory results were - Potassium of 2.2 mmol/L (3.5-5.1 mmol/L), chloride 73 mmol/L (98-107 mmol/L), Bicarbonate 50 mmol/L (22-29 mmol/L), Blood urea 22 mg/dl (9.8-20.1 mg/dl), Cr 1.4 mg/dl (0.5-1.0 mg/dl), total calcium of 16.6 mg/dl (9-11 mg/dl), ionized calcium 2.02 mmol/L (1.15-1.33 mmol/L), PTH was low to 8.9 pg/ml (10-65 pg/ml). Arterial blood gas showed metabolic alkalosis. Extensive evaluation to find the cause of hypercalcemia was negative. Detailed history after initial stabilization, revealed that she had been taking 10 tablets of calcium carbonate tablets per day and 1 glass of milk daily for reflux symptoms for the last eight weeks. Based on the history and after ruling out all the other serious causes, diagnosis of milk alkali syndrome was made and patient was discharged with proton pump inhibitor with advice to avoid calcium carbonate. Her hypercalcemia responded well to fluid resuscitation.Conclusions: Milk alkali syndrome once a rare cause of hypercalcemia has emerged as a third leading cause of hypercalcemia in completely different scenario. It is important to evaluate the patient with proper history including the use of over the counter calcium supplements to determine the etiology of hypercalcemia. Our case highlights the importance of proper history taking in the evaluation of hypercalcemia and that not all the cause of severe hypercalcemia is secondary to malignancy.

Renal infarction is a very rare disease. Due to the non-specific clinical presentation, diagnosis is often missed or delayed. As the result, a prolonged period of ischemia and irreversible renal damage is common. The broad availability of high-quality computed tomography (CT) imaging has made it possible to identify the cases early and initiate prompt treatment. We report a case of renal infarction that presented with acute abdomen. A 56-year-old man with the medical history of hypertension and diabetes mellitus presented to emergency department with a complaint of sudden onset of severe right lower abdominal pain for 1 day. CT scan of abdomen with contrast showed the striated appearance of the right kidney with hypoperfusion and wedge-shaped hypodensities throughout the kidney. After an extensive workup, no apparent cause of renal infarct was found. Due to the absence of underlying cause of atrial fibrillation or hypercoagulable disorder, no anticoagulation was started and he was discharged home on aspirin. Although the incidence of renal infarction is uncommon, it should always be suspected in the patient presenting with flank pain with nausea, vomiting, and fever, especially in presence of risk factor like atrial fibrillation and elevation of lactose dehydrogenase (LDH) with normal or mildly elevated aminotransferases. Early diagnosis and management of renal infarction is important to prevent a prolonged period of ischemia and irreversible damage. World J Nephrol Urol. 2018;7(2):53-55 doi: https://doi.org/10.14740/wjnu338e

Hyperostosis frontalis interna (HFI) is characterized by excess growth of the frontal bone. Although the exact cause of HFI is not known, it has been found to be associated with increased age, prolonged estrogen stimulation and elevated leptin. Literature shows its association with seizure, dementia, obesity, headache and endocrine abnormalities. HFI may be syndromic and non-syndromic. Timely identification of HFI can prevent unnecessary diagnostic tests. We report a case of non-syndromic HFI in an elderly female who presented with headache.

Hyperostosis frontalis interna (HFI) is characterized by excess growth of the frontal bone. Although the exact cause of HFI is not known, it has been found to be associated with increased age, prolonged estrogen stimulation and elevated leptin. Literature shows its association with seizure, dementia, obesity, headache and endocrine abnormalities. HFI may be syndromic and non-syndromic. Timely identification of HFI can prevent unnecessary diagnostic tests. We report a case of non-syndromic HFI in an elderly female who presented with headache.

A 47-year-old woman had been hospitalized one month earlier for lupus nephritis with a hypertensive emergency that led to a seizure. During this earlier hospitalization, she was given a diagnosis of posterior reversible encephalopathy syndrome.

Renal infarction is a serious medical emergency but its diagnosis is often delayed because it mimics many other conditionsincluding renal stones, pyelonephritis, renal cancer and back pain. Early diagnosis as well as treatment is important for preventingrecurrence of infarction and irreversible kidney damage. The most common causes of renal infarction are heart diseases leadingto embolism, renal trauma and atheromatous disease. However, in some patients, the etiology remains unclear and is labeled asidiopathic renal infarction. We report an unusual case of right lower abdominal pain which was finally determined to idiopathicrenal infarction after extensive investigation.