ObjectiveIn this study, we aimed to determine whether plasma NGAL levels could be used as a biomarker for distinguishing between AKI and CKD in emergency medicine.Materials and methodsThis prospective study was conducted at the ED of a training and research hospital over a six-month period in 2015. Three groups were defined: an AKI group – defined as a new onset of at least a 1.5-fold or ≥0.3 mg increment increase of SCr values from the normal baseline, a stable CKD group – only included presence of stages 2 through 4 of CKD according to the National Kidney Foundation's KDIGO 2012, and a control group. After the initial evaluation of patients, venous blood samples were taken for routine biochemical, counter blood cell, and plasma NGAL measurement at admission.ResultsA total of 25 patients with AKI, 22 patients with stable CKD, and 22 control subjects were enrolled. Level of plasma NGAL in AKI group was higher than those of the stable CKD group (median: 794 ng/ml IQR: 317–1300 & 390 ng/ml IQR: 219–664, p < 0.001). AUC was measured as 0.68 (p = 0.02, 95% CIs: 0.54–0.84) to assess the utility of plasma NGAL levels at varying cut-off values for distinguishing between AKI and CKD. For plasma NGAL, the best cut-off level was found to be 457 ng/ml (sensitivity: 72.0%, specificity: 64%).ConclusionThis study has clearly demonstrated that plasma NGAL levels were higher in AKI patients than in CKD patients. However, in clinical practice, the use of plasma NGAL levels to distinguish between AKI and CKD is limited.
Background: Accurate electrocardiogram (ECG) interpretation is key to quickly providing attention to patients, and the first health staff who evaluate ECGs are nurses. Method: This was a prospective study with a pre–posttest design. The study test included 15 ECGs related to primary cardiac arrhythmias. After pretest nurses were instructed on arrhythmia interpretation using the Cardiac Rhythm Identification for Simple People (CRISP) method, posttests were completed. Results: There was a significant difference between the pretest scores of nurses who had postgraduate education on ECG interpretation and who did not ( p = .002). Median test score increased from 3 (interquartile range [ IQR ] = 2–5) to 7 ( IQR = 5–9) ( p < .001). Participants mostly missed questions about heart blocks and were most successful with questions about fatal arrhythmias after education. Conclusion: The CRISP method is an effective, simple, and easy method for accurate ECG interpretation by nurses. The posttest scores of the participants, especially accurate interpretation of fatal arrhythmias, increased significantly after training. [ J Contin Educ Nurs . 2020;51(12):574–580.]
IntroductionCarbon monoxide (CO) poisoning is a health problem that frequently occurs in Turkey and worldwide. In Turkey, it accounts for 30% of the poisoning cases that end with death (1).This colorless, odorless, tasteless, and nonirritating gas is produced as a result of the incomplete burning of organic matter that can easily be absorbed by the lungs. CO poisoning can cause cerebral, cardiac, and general ischemia. The poisoning can be diagnosed according to the blood carboxyhemoglobin (COHb) levels. There is a weak correlation between blood COHb levels and organ damage. Poisonings higher than 60% end with death and at lower levels clinical findings range from mild to severe. It is not always possible to identify this using the COHb level (2). Biochemical markers other than COHb are being studied to identify the clinical outcomes of this poisoning with neurotoxic and cardiotoxic effects in particular (3).Copeptin is excreted from the posterior hypophysis simultaneously with vasopressin and reflects the amount of vasopressin in circulation. Copeptin is more stable than vasopressin in plasma and serum. Studies conducted have reported that copeptin and vasopressin levels float parallel to each other both in healthy individuals and in the critically ill patient population. Recently copeptin has been investigated as a diagnostic and prognostic factor in many diseases like pneumonia, heart failure, and hemorrhagic and septic shock and it has been identified that its levels rise in correlation with the severity of the disease (4-7).The aim of this study is to identify the copeptin levels in patients presenting to the emergency department with CO poisoning and to investigate its correlation with neurological damage.Background/aim: The aim of this study is to identify the copeptin levels in patients presenting with carbon monoxide (CO) poisoning to the emergency department and to investigate its correlation with the neurological effects. Materials and methods:The study group consisted of patients presenting with CO poisoning and carboxyhemoglobin levels >10%. Blood samples for copeptin levels were obtained twice, first at presentation then at the fourth hour of observation. The data were analyzed using SPSS 16 for Windows. Results:The median copeptin levels of the patient group were identified as 0.63 (0.39-1.06) ng/mL at hour 0 and 0.41 (0.31-0.49) at hour 4. The copeptin levels of the control group were 0.34 (0.25-0.42) ng/mL and were significantly lower than those of the patient group (P < 0.000). According to our results, 0.345 ng/mL for plasma copeptin level as the best cut-off level may be used with sensitivity of 94.0% and specificity of 60%. The copeptin levels at hour 0 were statistically significantly higher in the neurologically affected patients than those not affected (P < 0.001). Conclusion:In this study it was shown that blood copeptin levels increase in patients presenting to the emergency department with CO poisoning.
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