Diabetic ketoacidosis masked by both Euglycemia and a primary metabolic alkalosis.

Diabetic ketoacidosis (DKA) is an acute, life-threatening metabolic complication of diabetes classically associated with hyperglycemia, metabolic acidosis, and ketosis. Though relatively uncommon, patients can also develop DKA with relative euglycemia, further complicating diagnosis. Here, we describe the case of a patient who presented with intractable vomiting secondary to diabetic gastroparesis. He was euglycemic, non-acidemic, and serum bicarbonate was within normal limits. However, labs were significant for ketonuria, an elevated anion gap, and an elevated beta-hydroxybutyrate. Given the high concern for euglycemic DKA in the setting of a competing primary metabolic alkalosis, he was transferred to the intensive care unit for intravenous insulin infusion and fluid resuscitation with significant clinical improvement and normalization of laboratory results. This serves as an important reminder that DKA can be masked by euglycemia as well as additional metabolic derangements, and should be suspected in any diabetic patient with an anion gap and/or ketosis.

Case report: Rapid onset, ischemic-type gastritis after initiating oral iron supplementation.

Oral iron supplements are commonly administered to patients with chronic iron deficiency anemia. This approach is generally well-tolerated, causing only mild adverse effects. Rarely, oral iron supplementation can cause more severe symptoms, one of the most concerning being acute gastritis. This predominantly affects elderly patients and is extremely uncommon in young, otherwise healthy people. Here, we report the case of a 43-year-old woman who presented with upper gastrointestinal (GI) symptoms and iron deficiency anemia and was started on oral iron supplementation following the resolution of her acute symptoms. She soon re-presented with a severe, Helicobacter pylori-negative gastritis with iron deposition on histology. These new onset symptoms resolved rapidly with cessation of iron supplements, consistent with iron pill gastritis. In addition to the limited body of literature describing iron pill gastritis, this case serves as a reminder that any patient receiving oral iron supplementation is at a potential risk for gastritis, particularly in the setting of an ongoing GI pathology. Hence, it is important to provide continued follow-up for patients receiving iron supplementation regardless of age or comorbidity, particularly in the weeks following the start of the treatment.

Hospitalist Perspectives of Available Tests to Monitor Volume Status in Patients With Heart Failure: A Qualitative Study.

Acute decompensated heart failure is the leading admitting diagnosis in patients 65 years and older with more than 1 million hospitalizations per year in the US alone. Traditional tools to evaluate for and monitor volume status in patients with heart failure, including symptoms and physical exam findings, are known to have limited accuracy. In contrast, point of care lung ultrasound is a practical and evidenced-based tool for monitoring of volume status in patients with heart failure. However, few inpatient clinicians currently use this tool to monitor diuresis. We performed semi-structured interviews of 23 hospitalists practicing in five geographically diverse academic institutions in the US to better understand how hospitalists currently assess and monitor volume status in patients hospitalized with heart failure. We also explored their perceptions and attitudes toward adoption of lung ultrasound. Hospitalist participants reported poor reliability and confidence in the accuracy of traditional tools to monitor diuresis and expressed interest in learning or were already using lung ultrasound for this purpose. The time required for training and access to equipment that does not impede workflow were considered important barriers to its adoption by interviewees.

Unlikely culprit: congenital middle aortic syndrome diagnosed in the sixth decade of life.

A 58-year-old woman was admitted with acute heart failure. She had a long history of resistant hypertension, with an unremarkable work up for secondary causes in the past. Her brachial blood pressure was 210/70 mm Hg, with ankle blood pressure of 100/70 mm Hg. CT angiogram revealed marked narrowing of the descending thoracic aorta between the left subclavian artery and the diaphragm, consistent with middle aortic syndrome (MAS). She was initially managed with diuretics and antihypertensives. Subsequently thoracotomy revealed a severely hypoplastic segment of the descending aorta. The diseased segment was resected and aortic reconstruction performed. Histopathology showed fragmentation of the medial elastic fibres and fibrosis of the medial and intimal layers. These findings along with gross aortic hypoplasia and absence of features of Takayasu's arteritis, suggest that our patient had congenital MAS. The patient has done well since her surgery. We believe this is the first case of congenital MAS reported in the sixth decade of life.

Inferior vena cava diameter change after intravenous furosemide in patients diagnosed with acute decompensated heart failure.

PURPOSE: Measurement of the inferior vena cava (IVC) diameters may improve decision-making for patients hospitalized with acute decompensated heart failure. Nevertheless, little is known about how the IVC is affected by loop diuretics. We sought to determine if bolus infusions of intravenous furosemide affect IVC diameters measured by hand-carried ultrasonography. METHODS: We conducted a prospective cohort study at a public teaching hospital from September 2009 through June 2010. Physician investigators performed IVC ultrasonography on a convenience sample of 70 hospitalized adults who were prescribed intravenous furosemide for the diagnosis of acute decompensated heart failure. RESULTS: Participants' median baseline IVC diameter was 2.38 cm (interquartile range, 1.91-2.55 cm). At 1-2 hours after furosemide, IVC diameters decreased an average of 0.21 cm (95% CI, 0.13-0.29 cm) and remained significantly below baseline at 2-3 hours after furosemide by an average of 0.15 cm (95% CI, 0.07-0.22 cm). CONCLUSIONS: IVC diameters of adults diagnosed with acute decompensated heart failure become measurably smaller after single doses of intravenous furosemide. Whether this represents a true change in volume status has not been studied.