The treatment of quetiapine and/or citalopram poisoning is mainly supportive and involves gastric lavage, activated charcoal, intubation, and mechanical ventilation. Recently, however, there were reports of successful treatment with intravenous lipid emulsion. Here we report a case of a 19-year-old Caucasian girl who ingested approximately 6000 mg of quetiapine, 400 mg of citalopram, and 45 mg of bromazepam in a suicide attempt. The patient developed ventricular tachycardia and epileptic seizures 12 h after admission to the hospital. As the patient's condition deteriorated, we combined standard therapy (intubation, mechanical ventilation, and vasopressors) with low-dose intravenous lipid emulsion (ILE) (a total of 300 mL of 20 % lipid emulsion) and normalised her heart rhythm and stopped the seizures. She was discharged to the psychiatric ward after 48 h and home after a prolonged (2-month) psychiatric rehabilitation. Intravenous lipid emulsion turned out to be effective even in the lower dose range than previously reported for quetiapine poisoning in patients presenting with seizure and ventricular arrhythmia. To our knowledge, there are no case reports describing the use of ILE in treating citalopram poisoning. KEY WORDS: cardiac arrhythmias; complementary therapies; emergency treatment; epilepsy; poisoningSevere poisoning with quetiapine or citalopram can lead to life-threatening dysrhythmias and epileptic seizures. Therapy is mainly supportive (1-2). In recent years, there have been reports of successful use of intravenous lipid emulsions (ILE) to counter poisoning with lipophilic drugs, mainly local anaesthetics, beta blockers, and calcium channel blockers (3), including quetiapine (4-6). Here we present a patient with severe poisoning with quetiapine and citalopram (yet another lipophilic substance), who was successfully treated with ILE in the lower dose range than reported in most cases. CASE REPORTA 19-year-old girl was admitted to the hospital after having ingested about 6000 mg of quetiapine (20 300-mg tablets), 400 mg of citalopram, and 45 mg of bromazepam in a suicide attempt. The doses of ingested drugs were determined from medical history and empty packaging. On admission the patient was aroused; her Glasgow coma scale was 11, blood pressure 128/60 mmHg (17.1/8 kPa), and peripheral oxygen saturation without supplemental oxygen was 95 %. The pupils were dilated, symmetrical, and poorly reactive to light. Electrocardiogram revealed sinus tachycardia with the heart rate of 150 min -1 , incomplete right bundle branch block, and prolonged corrected QT interval of 510 ms. We performed gastric lavage, applied activated charcoal, and drew urine for toxicology testing, which turned positive for quetiapine and citalopram. The concentrations of quetiapine and citalopram were not determined.Twelve hours after the admission, we registered monomorphic premature ventricular contractions (PVCs) and generalised epileptic seizures. During the hour that followed, PVCs became more frequent and progressed to ventricul...

Atherosclerosis is a leading cause of morbidity and mortality in hemodialysis (HD) patients. Low (<0.90) and high (>1.40) ankle-brachial index (ABI) is known as a non-invasive diagnostic marker for generalized atherosclerosis associated with higher cardiovascular (CV) mortality in the general population. Less is known about associations between ABI and CV mortality in HD patients. The aim of our study was to determine the impact of the ABI on CV mortality in nondiabetic HD patients. Fifty-two nondiabetic HD patients (mean age 59 years, range 22 - 76 years) were enrolled in our study. Twenty-three (44%) were women and 29 (56%) men. The ABI was determined using an automated, non-invasive, waveform analysis device. All patients were divided according to the ABI into three groups: low ABI (<0.9), normal ABI (0.9-1.4) and high ABI (>1.4). The presence of arterial hypertension and smoking was established. Serum cholesterol (HDL and LDL) and triglycerides were measured by routine laboratory methods. Survival rates were analyzed using Kaplan-Meier survival curves. The Cox regression model was used to assess the influence of the ABI on CV outcomes. The model was adjusted for age, arterial hypertension, smoking, cholesterol and triglycerides. Mean ABI value was 1.2 ± 0.3 (range 0.2-2.2). Patients were observed from the date of the ABI measurement until their death or maximally up to 1620 days. Kaplan-Meier survival analysis showed that the risk for CV death was higher for HD patients with low and high ABI compared to normal ABI (log rank test: P < 0.006; P < 0.0001). In the adjusted Cox multivariable regression model low and high ABI (P < 0.011; P < 0.003) remained predictors of mortality in our patients. The results indicate a U-shaped association between the ABI and CV mortality in nondiabetic HD patients and showed that low and high ABI were directly associated with higher mortality of our patients.

Low (<0.9) and high (>1.4) ankle brachial index (ABI) is associated with a higher cardiovascular (CV) mortality in the general and hemodialysis (HD) population. The aim of our study was to determine the impact of ABI on long-term survival of 52 non-diabetic HD patients. The ABI was determined using an automated, non-invasive waveform analysis device. Patients were divided into three groups: low (<0.9), normal (0.9-1.4) and high (>1.4) ABI. Patients were observed from the date of ABI measurement until their death or ten years. Survival analysis showed higher risk for CV death in HD patients with high ABI compared to normal ABI (log rank test P < 0.027). In Cox regression model adjusted for arterial hypertension, smoking, serum cholesterol and triglycerides, high ABI (P < 0.049) remained a predictor of mortality. The results indicate an association between ABI and long-term survival of non-diabetic HD patients and only high ABI was associated with higher CV mortality.

Purpose: Abdominal adipose tissue has important inflammatory properties and is a source of various inflammatory mediators. Given that concentrations of some inflammatory mediators are high among hemodialysis (HD) patients, abdominal obesity may play an important role in the pathogenesis of microinflammation which is known to be associated with accelerated atherosclerosis. The aim of our study was to determine the impact of microinflammation on cardiovascular (CV) mortality in abdominal obese HD patients. Methods: Seventy–one HD patients (mean age 59.3 ± 12.8 years) were included in our study. Waist circumference (WAC) was measured and abdominal obesity was defined according to the International Diabetes Federation. Serum levels of lipids (triglycerides, high density lipoproteins (HDL) cholesterol, low density lipoproteins (LDL) cholesterol) and inflammatory mediators (interleukin–6, tumor necrosis factor–alpha, vascular cellular adhesion molecule–1 (VCAM–1), intercellular adhesion molecule–1 (ICAM–1)) were measured. Patients were observed from the date of measurement (November 2003) of inflammatory mediators until their death or to 10th of November 2009. Results: The mean WAC value for men was 97.6 ± 16.1 cm, and for women 92.2 ± 15.9 cm. Abdominal obesity was found in 62% of the enrolled patients. Cox regression analysis showed that the inflammatory mediators VCAM–1 (p<0.031) and ICAM–1 (p<0.024) were predictors of CV mortality in abdominal obese HD patients. Both inflammatory mediators remained predictors of CV mortality if age and other known risk factors for atherosclerosis (arterial hypertension, smoking, HDL and LDL cholesterol and triglycerides) were included in the analysis. Conclusion: The results of our study indicate that microinflammation is associated with CV mortality in abdominal obese HD patients.

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