Orthostatic Signs Research Articles

The Clinical and Electroencephalographic Spectrum of Tilt-Induced Syncope and “Near Syncope” in Youth

BackgroundThe aim of the study was to characterize the clinical and electroencephalographic (EEG) patterns associated with tilt-induced reflex syncope and delayed orthostatic hypotension without syncope in youth. MethodsWe conducted a prospective observational study of 95 patients referred to a pediatric neurology clinic for head-upright tilt testing. Clinical signs, symptoms, video EEG, and continuous blood pressure and heart rate were monitored. ResultsEighty patients had reflex syncope, and 15 had delayed-onset hypotension without syncope. The mean age was 15.3 (standard deviation ±2.3) years; 75 (78.9%) were female. All patients with hypotension only had corresponding signs and symptoms; 13 (86.7%) had corresponding EEG slowing. The duration of EEG slowing with hypotension far exceeded the presyncope interval from onset of slowing to loss of consciousness among patients with syncope (P < 0.001). Although prior near-syncope and presyncope episodes were reported commonly in both groups, patients with delayed hypotension without syncope were less likely to have experienced loss of consciousness during episodes of orthostatic intolerance (P < 0.001). Patients with syncope had either slow-flat-slow (n = 23) or slow-only (n = 57) EEG patterns. Compared to those with slow-only EEG patterns, patients with the slow-flat-slow pattern had greater rates of asystole (P < 0.001), myoclonic movements (P < 0.001), facial grimace (P = 0.003), vocalizations (P = 0.002), and arm flexion (P < 0.001) or extension (P = 0.006) during tilt-induced syncope. ConclusionsAmong otherwise healthy youth, orthostatic signs and symptoms vary across the spectrum of tilt-induced reflex syncope and delayed hypotension without syncope. Delayed hypotension without syncope may represent the poorly defined phenomenon of “near syncope” in some patients.

Renal failure associated with Legionella pneumophila infection

A 61-year-old African-American male with a past medical history of hypertension and osteoarthritis was brought to the emergency department for severe dyspnoea and agitation for the past few hours. Family members gave a history of fever, myalgias, anorexia, nausea and a non-productive cough of 3–4 days duration. He also had a several day history of shortness of breath and right-sided pleuritic chest pain. He had a 40-pack a year tobacco history and consumed 1–2 beers every day. He had had no alcohol in the past 4 days. His home medications included amlodipine and ibuprofen. He was currently unemployed. In the emergency department, vitals signs included a temperature of 38.8°C, pulse rate of 118 beats per minute, respiratory rate of 24 breaths per minute, blood pressure of 122/68 mmHg with no orthostatic signs and an oxygen saturation of 89% on 4 litres oxygen by nasal cannula. Physical examination was unremarkable except for intermittent agitation and crackles on auscultation of the right middle and lower lung zones. Laboratory values at admission were as follows: sodium =129 mmol/litre, bicarbonate =23 mmol/litre, blood urea nitrogen = 30.7 mmol/litre, creatinine = 910.5 μmol/litre, total bilirubin =80.4 μmol/litre with an unconjugated fraction of 53 μmol/litre, alkaline phosphatase = 110 U/litre, alanine transaminase = 147 U/litre, aspartate aminotransferase = 234 U/litre, creatine kinase = 7533 U/litre with muscle-brain fraction of 7.48 U/litre, haemoglobin = 129 g/litre, white blood cell count = 10100/mm3 with 43% bands, platelet count = 200 000/mm3, other labs including serum calcium, magnesium, chloride, potassium, phosphate, amylase and lipase were within the normal range. Serum and urine toxicological screens were negative. Electrocardiogram revealed normal sinus rhythm with left ventricular hypertrophy by voltage criteria. Urine dipstick was positive for large amount of blood. Urine microscopy showed 110 red blood cells per high power field. A chest roentgenogram showed a right lower lobe infiltrate. Upon admission, the patient's hypoxaemia worsened and he required bi-level positive airway pressure for ventilation. With a presumptive diagnosis of aspiration pneumonia vs community-acquired pneumonia, piperacillin-tazobactam and azithromycin were instituted. In view of the agitation and the patient's history of alcohol use, he was placed on alcohol withdrawal precautions. Renal service was consulted the following morning for his non-oliguric acute renal failure (urine output = 600 ml over the previous 24 hours). The baseline renal function of this patient was not known. With evidence of multiple organ system involvement including the lungs, liver and kidney, an extensive work-up for vasculitides as well as an infectious aetiology was initiated. Serum complement levels (C3, C4, and CH 50) were within the normal range. Assays for anti-nuclear antibody, anti-double-stranded DNA antibody, anti-neutrophilic cytoplasmic antibodies, anti-glomerular basement membrane antibody as well as serological tests for hepatitis B and C were all negative. Renal failure worsened over the next 3 days and the patient required hemodialysis three times over the next 4days (Figure 1). While all tests including sputum, urine and blood cultures remained negative, the urinary antigen for Legionella pneumophila serogroup 1 was positive. Piperacillin-tazobactam was discontinued and azithromycin was continued to complete a 21-day course. Serum creatinine at discharge was 300.5 μmol/litre. The patient was subsequently lost to follow-up.