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Background/aims Limited data exists on the outcomes of COVID-19 patients presenting with altered mental status (AMS). Hence, we studied the characteristics and outcomes of hospitalized COVID-19 patients who presented with AMS at our hospital in rural southwest Georgia. Methods Data from electronic medical records of all hospitalized COVID-19 patients from March 2, 2020, to June 17, 2020, were analyzed. Patients were divided in 2 groups, those presenting with and without AMS. Primary outcome of interest was in-hospital mortality. Secondary outcomes were needed for mechanical ventilation, need for intensive care unit (ICU) care, need for dialysis, and length of stay. All analyses were performed using SAS 9.4 and R 3.6.0. Results Out of 710 patients, 73 (10.3%) presented with AMS. Majority of the population was African American (83.4%). Patients with AMS were older and more likely to have hypertension, chronic kidney disease (CKD), cerebrovascular disease, and dementia. Patients with AMS were less likely to present with typical COVID-19 symptoms, including dyspnea, cough, fever, and gastrointestinal symptoms. Predictors of AMS included age ≥ 70 years, CKD, cerebrovascular disease, and dementia. After multivariable adjustment, patients with AMS had higher rates of in-hospital mortality (30.1% vs 14.8%, odds ratio (OR) 2.139, p = 0.019), ICU admission (43.8% vs 40.2%, OR 2.59, p < 0.001), and need for mechanical ventilation (27.4% vs 18.5%, OR 2.06, p = 0.023). Patients presenting with AMS had increased length of stay. Conclusions Patients with COVID-19 presenting with AMS are less likely to have typical COVID-19 symptoms, and AMS is an independent predictor of in-hospital mortality, need for ICU admission, and need for mechanical ventilation.

A collaborative study compared methods for measuring glycosylated haemoglobin in seven laboratories in the United Kingdom. No satisfactory standard for general use was found. Satisfactory internal quality control systems were in use for each assay which allowed the maintenance of a normal range in each participating laboratory. No satisfactory quality control system suitable for general use could be identified. Costs and convenience of the assays are reported. The technical problems with each type of assay and precautions for their use were identified, such as the need for standardization in incubation times, the practicability of automation of colorimetric assays, and the precision of pH needed for buffers in column separation methods. The relevance of the technical problems to interpretation of measurements is also considered. It is concluded that laboratories measuring glycosylated haemoglobin should maintain a normal range, use 'in-house' quality controls to monitor assay performance and keep clinical colleagues informed of the findings and of any changes in methodology that might affect the interpretation of results.

Changes in plasma gastrin and lower oesophageal sphincter pressure were measured in 20 subjects after a standard protein meal. Significant increases in both gastrin and sphincter pressure were seen. Peak gastrin response occurred an average of 19-5 minutes and peak lower oesophageal sphincter response 40-0 minutes after the meal. Both gastrin and sphincter pressure showed a wide spectrum of response. In 5 subjects there was no appreciable rise (less than 5 pg/ml) in plasma gastrin after the meal, and 3 of these had symptoms of oesophageal reflux. In this group there was only a small but nervertheless significant rise in lower oesophageal sphincter pressure (mean pressure rise 18-0 per cent of fasting value, p less than 0.05). Greater increases in sphincter pressure (mean rise 54-2 per cent, p less than 0.005) were seen in subjects with a moderate (up to 50 pg/ml) rise in plasma gastrin, and those with the most marked gastrin response (less than 50 pg/ml) showed the greatest rise in pressure (mean rise 80-3 per cent, p less than 0.0025). These results suggest that endogenous plasma gastrin is the main stimulus to the rise in lower oesophageal sphincter pressure after food. Subjects with a poor gastrin response to the meal have only a small increase in sphincter pressure and as a result may be more liable to develop gastro-oesophageal reflux.

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