I read with interest the study of Raluca Fodor et al., on the significance of Plasma Neutrophil Gelatinase-Associated Lipocalin (NGAL), as an early biomarker for acute kidney injury in critically ill patients, published recently in issue no.4/2015 of JCCM journal . In this well-written and interesting study, the authors successfully demonstrated that in critically ill patients, increased levels of NGAL predict, with a good sensitivity and specificity, the development of acute kidney injury within forty-eight hours of admission to an ICU. However, as no information is presented on the aetiology of the acute kidney injury, we believe that the article raises interesting and still un-elucidated hypotheses on the pathophysiological substrate of the systemic release of NGAL in patients with critical conditions. [More]
Staphylococcal toxic shock syndrome (STSS) represents a potentially lethal disease, and survival depends primarily on the early initiation of appropriate treatment. As the clinical picture at presentation is usually common, frequently this could lead to misdiagnosis and delays in the initiation of the proper therapy. The case of a 43-years old female who developed a staphylococcal septic shock syndrome caused by a forgotten intravaginal tampon is reported.
Introduction: It has been reported that as compared with total intravenous anesthesia (TIVA), inhalation anesthesia is increasing the postoperative level of proinflammatory interleukins.
The aim of the study is to investigate if there is an in-vivo relationship between proinflammatory cytokines, Interleukin-32 (IL-32) and Tumour necrosis factor – α (TNF- α), in patients undergoing laparoscopic cholecystectomies with two different anesthetic techniques, TIVA or inhalation anesthesia.
Material and Methods: Twenty two consecutive patients undergoing laparoscopic cholecystectomies were prospectively randomized into two groups: Group 1: TIVA with target-controlled infusion (TIVA-TCI) (n=11) and Group 2: isoflurane anesthesia (ISO) (n=11). IL-32 and TNF-α were determined before the induction of anesthesia (T1), before incision (T2) and at 2h (T3) and 24h (T4) postoperatively. Our primary outcome was to compare plasma levels of IL-32 and TNF- α concentrations (expressed as area-under-the-curve) over 24 hours between study groups. Our secondary outcome was to establish whether there is a correlation between plasma levels of IL-32 and of TNF-α at each time point between the two groups.
Results: Area-under-the-curve (AUC) of IL-32 plasma concentration was 7.53 in Group 1 (TIVA) versus 3.80 in Group 2 (ISO), p= 1. For TNF-α, AUC of plasma concentration was 733.9 in Group 1 (TIVA) and 668.7 in Group 2 (ISO), p= 0.066. There were no significant differences in plasma concentrations of both IL-32 and TNF- α between the groups.
Conclusions: IL-32 expression in response to minor surgery is very low. There were no significant difference between plasma levels ofTNF- α and IL-32 after TIVA versus inhalation anesthesia during the first 24 hours postoperatively. Further studies are needed on larger groups to investigate whether there can be a correlation between these interleukins after 2 different anesthetic techniques and the impact of this correlation on postoperative outcome.
Clostridium difficile, an anaerobic, spore-forming, toxin-forming, gram-positive bacillus present in the bacterial flora of the colon is the principal cause of nosocomial diarrhoea in adults.
Aim: Assessment of favouring factors of Clostridium difficile infections as well as the interactions between them, in critically ill hospitalized patients undergoing complex medical and surgical treatments.
Material and Methods: A retrospective case-control study involving eighty patients admitted in the Intensive Care Unit (ICU) of the County Clinical Emergency Hospital Tîrgu-Mureş was conducted between January and October 2014. Patients aged eighteen years and over, who had undergone complex medical and surgical treatment, were divided into two subgroups. Group 1 included patients who developed diarrhoea but were not diagnosed as having a Clostridium difficile infection (CDI). Group 2 included patients who developed diarrhoea due to CDI as indicated by a positive culture and the expression of exotoxin. The assessed parameters were age, length of stay (LOS), antibiotic spectrum, association with proton pump inhibitors (PPI) or H2-receptor antagonists, immunological status, the presence or lack of gastrointestinal tract surgery.
Results: The mean age was 64.6 years with an average LOS of 10 days. Fifty-six percent of patients came to the ICU from internal medicine wards and forty-three percent from surgical wards. 20.5% of them were immunosuppressed. Co-association of ceftriaxone and pantoprazole significantly increased the risk of CDI compared to co-administration of any other antibiotic or pantoprazole (p=0.01). The odds ratio for Pantoprazole together with any antibiotic versus antibiotic therapy alone was significantly higher (p=0.018) with a sevenfold increase in the risk of positive exotoxin increase.
Conclusions: Antibiotic use is associated with “no risk to develop CDI” in the first five days of administration. PPIs associated therapy increased the risk of CDI in first seventy-two hours regardless of the antibiotic type, and contributes to an active expression of CD exotoxin.
Mucosal capnometry involves the monitoring of partial pressure of carbon dioxide (PCO2) in mucous membranes. Different techniques have been developed and applied for this purpose, including sublingual or buccal sensors, or special gastrointestinal tonometric devices. The primary use of these procedures is to detect compensated shock in critically ill patients or patients undergoing major surgery. Compensatory mechanisms, in the early phases of shock, lead to the redistribution of blood flow towards the vital organs, within ostensibly typical macro-haemodynamic parameters. Unfortunately, this may result in microcirculatory disturbances, which can play a pivotal role in the development of organ failure. In such circumstances mucosal capnometry monitoring, at different gastrointestinal sites, can provide a sensitive method for the early diagnosis of shock. The special PCO2 monitoring methods assess the severity of ischaemia and help to define the necessary therapeutic interventions and testing of these monitors have justified their prognostic value. Gastrointestinal mucosal capnometry monitoring also helps in determining the severity of ischaemia and is a useful adjunctive in the diagnosis of occlusive splanchnic arterial diseases. The supplementary functional information increases the diagnostic accuracy of radiological techniques, assists in creating individualized treatment plans, and helps in follow-up the results of interventions. The results of a pilot study focusing on the interrelation of splanchnic perfusion and gastrointestinal function are given and discussed concerning recent advances in mucosal capnometry.
Introduction: In patients with out-of-hospital cardiac arrest (OHCA) complicating an ST-segment elevation myocardial infarction (STEMI), the survival depends largely on the restoration of coronary flow in the infarct related artery. The aim of this study was to determine clinical and angiographic predictors of in-hospital mortality in patients with OHCA and STEMI, successfully resuscitated and undergoing primary percutaneous intervention (PCI).
Methods: From January 2013 to July 2015, 78 patients with STEMI presenting OHCA, successfully resuscitated, transferred immediately to the catheterization unit and treated with primary PCI, were analyzed. Clinical, laboratory and angiographic data were compared in 28 non-survivors and 50 survivors.
Results: The clinical baseline characteristics of the study population showed no significant differences between the survivors and non-survivors in respect to age (p=0.06), gender (p=0.8), the presence of hypertension (p=0.4), dyslipidemia (p=0.09) obesity (p=1), smoking status (p=0.2), presence of diabetes (p=0.2), a clinical history of acute myocardial infarction (p=0.7) or stroke (p=0.17). Compared to survivors, the non-survivor group exhibited a significantly higher incidence of cardiogenic shock (50% vs 24%, p=0.02), renal failure (64.3% vs 30.0%, p=0.004) and anaemia (35.7% vs 12.0%, p=0.02). Three-vessel disease was significantly higher in the non-survivor group (42.8% vs. 20.0%, p=0.03), while there was a significantly higher percentage of TIMI 3 flow postPCI in the infarct-related artery in the survivor group (80.% vs. 57.1%, p=0.03). The time from the onset of symptoms to revascularization was significantly higher in patients who died compared to those who survived (387.5 +/- 211.3 minutes vs 300.8 +/- 166.1 minutes, p=0.04), as was the time from the onset of cardiac arrest to revascularization (103.0 +/- 56.34 minutes vs 67.0 +/- 44.4 minutes, p=0.002). Multivariate analysis identified the presence of cardiogenic shock (odds ratio [OR]: 3.17, p=0.02), multivessel disease (OR: 3.0, p=0.03), renal failure (OR: 4.2, p=0.004), anaemia (OR: 4.07, p=0.02), need for mechanical ventilation >48 hours (OR: 8.07, p=0.0002) and a duration of stay in the ICU longer than 5 days (OR: 9.96, p=0.0002) as the most significant independent predictors for mortality in patients with OHCA and STEMI.
Conclusion: In patients surviving an OHCA in the early phase of a myocardial infarction, the presence of cardiogenic shock, renal failure, anaemia or multivessel disease, as well as a longer time from the onset of symptoms or of cardiac arrest to revascularization, are independent predictors of mortality. However, the most powerful predictor of death is the duration of stay in the ICU and the requirement of mechanical ventilation for more than forty-eight hours.
The purpose of this update is to provide recent knowledge and debates regarding the use of sugammadex in the fields of anesthesia and critical care. The review is not intended to provide a comprehensive description of sugammadex and its clinical use.
Out-of-hospital cardiac arrest (OHCA) remains associated with a poor prognosis, with a survival rate of approximately 10% . Only 40% of patients presenting with OHCA are successfully resuscitated, and only 25% of them survive to hospital discharge .
In many cases of OHCA associated with acute myocardial infarction, the cardiac arrest is caused by ventricular fibrillation, occurring during the first hours after the onset of symptoms, and before the patient being admitted to hospital . In these critical cases, implementation of specific protocols and dedicated networks are crucial for providing effective advanced cardiac life support.
Several treatment modalities have been proposed to improve outcomes in the post-resuscitation period. One such measure is induced therapeutic hypothermia, consisting of administering cooling infusions to cool the patient down to 32-34⁰C, and maintaining this for 12-24 hours. Evidence shows that when initiated promptly, cooling improves neurological outcomes in survivors of OHCA [3,4]. However, there is no clear evidence that hypothermia would lead to a significant reduction in mortality in these patients. Current guidelines recommend early therapeutic hypothermia as a class Ib indication, in the post-resuscitation phase, after cardiac arrest in patients who are comatose or deeply sedated . [More]
It is well known that critically ill patients require special attention and additional consideration during their treatment and management. The multiple systems and organ dysfunctions, typical of the critical patient, often results in different patterns of enteral absorption in these patients. Anti-platelet drugs are the cornerstone in treating patients with coronary and cerebrovascular disease. Dual anti-platelet therapy with aspirin and clopidogrel is the treatment of choice in patients undergoing elective percutaneous coronary interventions and is still widely used in patients with acute coronary syndromes. However, despite the use of dual anti-platelet therapy, some patients continue to experience cardiovascular ischemic events. Recurrence of ischemic events is partly attributed to the fact that some patients have poor inhibition of platelet reactivity despite treatment. These patients are considered low- or non-responders to therapy. The underlying mechanisms leading to resistance are not yet fully elucidated and are probably multifactorial, cellular, genetic and clinical factors being implicated. Several methods have been developed to asses platelet function and can be used to identify patients with persistent platelet reactivity, which have an increased risk of thrombosis. In this paper, the concept of anti-platelet therapy resistance, the underlying mechanisms and the methods used to identify patients with low responsiveness to anti-platelet therapy will be highlighted with a focus on aspirin and clopidogrel therapy and addressing especially critically ill patients.