Dizziness in the emergency department: an update on diagnosis.

This review aims to assist emergency physicians in finding the underlying aetiology when a patient presents with dizziness to the emergency department. After reading this review, the emergency physician will be able to consider the most relevant differential diagnoses and have an idea about dangerous aetiologies that require immediate action. The emergency physician will also know what diagnostic steps need to be taken at what time, such as the three-component HINTS Test (Head Impulse, Nystagmus, and Test-of-Skew), which helps with distinguishing central from peripheral causes of the acute vestibular syndrome. Furthermore, episodic vestibular syndromes and chronic vestibular syndromes are discussed in detail. The five most frequent categories of dizziness are vasovagal syncope / orthostatic hypotension (22.3%), vestibular causes (19.9%), fluid and electrolyte disorders (17.5%), circulatory/pulmonary causes (14.8%) and central vascular causes (6.4%). Given that it would neither be economical nor practical to send all patients to specialists from the start, we present general guidelines for the diagnostic workup of patients presenting with dizziness to the emergency department. This review will focus on epidemiology, aetiologies, differential diagnoses and diagnostics. Treatment is described in a separate article.

Emergency Presentations With Nonspecific Complaints-the Burden of Morbidity and the Spectrum of Underlying Disease: Nonspecific Complaints and Underlying Disease.

The prevalence of diagnoses, morbidity, and mortality of patients with nonspecific complaints (NSC) presenting to the emergency department (ED) is unknown.To determine the prevalence of diagnoses, acute morbidity, and mortality of patients with NSC.Prospective observational study with a 30-day follow-up. Patients presenting to 2 EDs were enrolled by a study team and diagnosed according to the World Health Organization ICD-10 System.Of 217,699 presentations to the ED from May 2007 through to February 2011, a total of 1300 patients were enrolled. After exclusion of 90 patients who fulfilled exclusion criteria, 1210 patients were analyzed. No patient was lost to follow-up. In patients with NSC, the underlying diseases were spread throughout 18 chapters of the ICD-10. A total of 58.7% of the patients were diagnosed with acute morbidity. Thirty-day mortality was 6.4% overall. Patients with acute morbidity and suffering from heart failure and pneumonia had mortalities >15%; patients lacking acute morbidity, but suffering from functional impairment or depression/anxiety had mortalities of 0%. Although the history did not allow any prediction, age and sex were predictive of morbidity and mortality.The differential diagnoses in patients presenting with NSC is broad. Acute morbidity and mortality were high in the presented cohort, the predictors of morbidity and mortality being age and sex rather than the nature of the complaints. Urgently needed management strategies could be based on these results.ClinicalTrials.gov (#NCT00920491).

Sildenafil in hypoxic pulmonary hypertension potentiates a compensatory up-regulation of NO-cGMP signaling.

The availability of inhibitors of cGMP-specific phosphodiesterase 5 (PDE 5), such as sildenafil, has revolutionized the treatment of pulmonary hypertension (PH). Sildenafil may exert its protective effects in a mechanism-based fashion by targeting a pathophysiologically attenuated NO-cGMP signaling pathway. To elucidate this, we analyzed changes in the pulmonary expression and activity of key enzymes of NO-cGMP signaling as well as the functional pulmonary responses to sildenafil in the 5 or 21 day hypoxia mouse model of PH. Surprisingly, we found doubled NO synthase (NOS) II and III levels, no evidence for attenuated NO bioavailability as evidenced by the nitrosative/oxidative stress marker protein nitro tyrosine, and no changes in the expression and activity of the NO receptor, soluble guanylyl cyclase (sGC). PDE 5 was either unchanged at day 5 or, after 21 days of hypoxia, even significantly decreased along with unchanged activity. Biochemically, these changes were mirrored by increased cGMP spillover into the lung perfusate and cGMP-dependent phosphorylation of the vasodilator-stimulated phosphoprotein, VASP. Sildenafil further augmented cGMP and phospho-VASP levels in lungs of mice exposed for 5 or 21 days and decreased pulmonary arterial pressure in mice after 5 days but not 21 days of hypoxia. In conclusion, NO-cGMP signaling is compensatorily up-regulated in the hypoxic mouse model of PH, and sildenafil further augments this pathway to functionally alleviate pulmonary vasoconstriction.