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OBJECTIVE: To assess the sensitivity and specificity of emergency physicians in detecting anxiety and depression in patients requiring admission to the emergency department (ED) observation care unit for complementary investigations/treatment. METHODS: 339 consecutive patients admitted to the emergency observation care unit of 14 EDs were interviewed with standardised questionnaires. The characteristics of the patients, EDs and attending ED physicians were collected. Patients' anxiety and depression were identified using the Hospital Anxiety and Depression Scale (HADS), a self-administered questionnaire. ED physicians were blind to the HADS score and were asked to declare whether they perceived anxiety and depression in each patient. The judgement of ED physicians and the HADS score were compared using sensitivity, specificity, positive and negative likelihood ratios. RESULTS: The HADS questionnaire was correctly completed by 310 patients who comprised the study population. HADS detected symptoms of anxiety in 148 patients (47%) and symptoms of depression in 70 patients (23%). ED physicians determined the presence or absence of anxiety with a sensitivity of 48% (95% CI 40% to 56%) and a specificity of 69% (95% CI 61% to 75%). Positive and negative likelihood ratios were 1.54 (95% CI 1.16 to 2.06) and 0.75 (95% CI 1.28 to 3.28) for anxiety. They detected the presence or absence of depression with a sensitivity of 39% (95% CI 28% to 51%) and a specificity of 78% (95% CI 72% to 83%). Positive and negative likelihood ratios were 1.75 (95% CI 1.20 to 2.56) and 0.78 (95% CI 1.26 to 3.87) for depression. CONCLUSION: Although patients presenting to the ED often experience anxiety and depression, these symptoms are poorly detected by ED physicians.

Critically ill patients often require emergency intubation. The use of etomidate as the sedative agent in this context has been challenged because it might cause a reversible adrenal insufficiency, potentially associated with increased in-hospital morbidity. We compared early and 28-day morbidity after a single dose of etomidate or ketamine used for emergency endotracheal intubation of critically ill patients.

Impaired oxygenation due to microcirculatory changes within the cerebral parenchyma may contribute to deterioration of intellectual function in vascular senile dementia (Hachinski score ≥ 7). The action of naftidrofuryl, used for treating elderly patients with senile dementia, was evaluated objectively in two groups of patients given naftidrofuryl either as a single intravenous dose or by chronic oral administration for three months. Their cerebral, microcirculatory flow rate was assessed before and after treatment by in vivo cineangioscintigraphy following an i.v. bolus of Tc-99m labelled erythrocytes. The deformability of erythrocytes from orally treated patients was also measured using an in vitro cellular transit time analyser (CTA) technique. A further experiment assessed the rheology of a rigid sub-population of erythrocytes in pathological samples when exposed to naftidrofuryl at concentrations appropriate to clinical use. Cerebral flow rates increased by about 20% and 30% after intravenous or chronic oral naftidrofuryl, respectively and these differences were statistically significant. In 10 orally treated patients, mean transit times by CTA decreased from 3.12 ms (day 0) to 2.70 ms (day 87 of treatment) (p<0.01). In the presence of naftidrofuryl, the proportion of the least deformable erythrocytes in pathological samples decreased by at least 50%. Clinical effects of naftidrofuryl on the cerebral microcirculation were not restricted to acute exposure. Naftidrofuryl may enhance the deformability of individual erythrocytes.

Tissue hypoxaemia can be evaluated by the noninvasive method of transcutaneous oxygen tension (tcpO2) measurement in patients with peripheral arterial occlusive disease (PAOD). The effects of naftidrofuryl (Praxilene®) on exercise-induced tissue ischaemia was objectively assessed by continuously measuring the tcpO2in 30 patients during three treadmill tests over a 3-month period in a randomized double-blind, placebo controlled, parallel group study. To be included in the study, the tcpO2and total walking distance had to be stable during the washout period (D-15-D0). The area under the tcpO2curves was scanned and automatically calculated after identification of baseline and the end of the treadmill test. The treadmill test on D30 and D90 was terminated at a similar walking distance to that obtained on D0. On D0 both groups were comparable (p = 0.22). The area under the curve (AUC) reduced significantly in the naftidrofuryl group between D0 and D30 (p, 0.001) and D0 and D90 (p, 0.001). However, no significant tcpO2AUC reduction was found in the placebo group (D0-D30, p = 0.58; D0-D90, p = 0.50). This was confirmed by calculation of the percentage of patients whose percentage change in the AUC on D90 was higher than the upper limit of the 90% confidence interval, calculated from the percentage change over the washout period. Of the 15 patients receiving naftidrofuryl, 66.6% exceeded this upper limit, compared with only 7% of patients receiving placebo (p = 0.0017). This study shows that naftidrofuryl has a protective effect on exercise-induced tissue ischaemia as measured by the tcpO2AUC in PAOD stage II patients.