Review Articles

One half of cortical thymoma patients develop myasthenia gravis (MG), an autoimmune disease affecting the voluntary muscles, while 15% of MG patients have thymomas. Thymectomy has been a mainstay in the treatment of myasthenia gravis and the management of such surgical patients is extremely demanding both at the physician’s and at the nurse’s level. In this paper we review some of the nursing interventions for patients with MG undergoing surgical removal of the thymus gland.

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Bloodstream infections (BSIs) are a frequent and life threatening condition in hospital settings. The case fatality rate associated with BSI reaches 35-50% when associated with admission to intensive care unit (ICU). The extensive use of intravascular catheters, however, is recognized as the most important factor contributing to the occurrence of BSI. Catheter-related BSIs (CR-BSIs) are the most common types of BSI in ICU. Bacteraemias that occur in the ICU are classified as Community Onset BSI and Hospital Acquired (HA) BSI. They are also distinguished in primary and secondary. Community-onset BSIs are those that occur in outpatients or are first identified 48 h after admission to hospital/ICU, and they may be sub classified further as health care associated (HCA), when they occur in patients with significant prior health care exposure, or community associated, in other cases. Hospital Acquired (HA) and / or ICU-acquired BSIs are defined as those occurring more than 48 hours after the patient's admission into the hospital or ICU or within 48 hours of leaving the hospital or the ICU. Community acquired BSIs usually due to susceptible bacteria should be clearly differentiated from HCA and HA BSIs frequently due to resistant hospital strains. A bedridden status, presence of indwelling devices, recent hospitalization or contact with health care facilities and recent antibiotic therapy may represent the most important risk factors for the development of emerging multi drug resistant (MDR) GN infections. The basic components of the treatment of a bacteraemia in the ICU are determining the type of bacteraemia in order to target potential pathogens, the initiation of empirical antimicrobial therapy based on the guidelines, and the source control if it is a secondary bacteremia. These goals become difficult to achieve in case of BSI due to multi-drug resistant pathogens with high MICs to antimicrobials. The main mechanisms which have put in danger the marvelous antibiotic weapon are the production of ESBL (several different subtypes), the production of carbapenemases and metallo-betalactamases, with consequent spread of multi or pan-resistant organism and the emerging growing resistance in colistin. The targeted treatment should be applied immediately after receiving the susceptibility test from the cultures. Targeted treatment essentially consists in redefining antibiotic treatment, in de-escalation in order to decrease the antibiotic selection pressure, and in determining the duration of treatment. Source control is recognized as an important part of the therapy of BSIs and has been recently shown to be independently related with outcome. Depending on the source of the infection (pneumonia, CRBSIs, urinary tract infections, intra-abdominal infections), the therapeutic strategy should be based on international guidelines in combination with local microbiology and local antibiotic resistance data.

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Increased intracranial pressure (ICP) is a serious final common pathway of a variety of neurologic injuries. Elevated ICP has consistently been associated with a poor outcome. It is a medical emergency requiring immediate intervention to prevent permanent damage to the brain. The Monro-Kellie doctrine states that the intracranial space is a fixed volume inside the skull. It describes the principle of homeostatic intracerebral volume regulation. The Monro-Kellie hypothesis and cerebral dynamics are important in order to understand the pathophysiology of intracranial hypertension. Venous occlusion, increased cerebral volume, increased blood volume, mass effect and cerebral edema are the major pathogenetic mechanisms of intracranial hypertension. The clinical manifestations of increased ICP are varied and unreliable. Headache, vomiting, disorientation, and lethargy are the main symptoms as well as symptoms and signs caused by cerebral herniation. ICP monitoring is widely used in clinical practice in order to improve patient outcome. It is especially useful as a robust predictor of cerebral perfusion, and can help to guide therapy and assess long‑term prognosis. Intraventricular catheters remain the gold standard for ICP monitoring, as they are the most reliable, accurate and cost‑effective, and allow therapeutic cerebrospinal fluid drainage. Intraparenchymal catheters are usually considered accurate, with the potential disadvantage that they measure localised pressure, which may not be reflective of global ICP. Furthermore, non‑invasive methods of ICP monitoring, such as transcranial Doppler, optic nerve sheath diameter, etc., have emerged as promising techniques for screening patients with raised ICP in settings where invasive techniques are either not feasible (patients with severe coagulopathy) or not available (setups without access to a neurosurgeon).

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Intracranial hypertension (IH) is currently managed in the intensive care unit with a combined medical – surgical approach. Progress in monitoring and in understanding pathophysiological mechanisms of IH could change current management in the intensive care unit, enabling targeted interventions that could ultimately improve outcomes. The prevention of secondary brain damage from raised intracranial pressure (ICP) is the central focus of neurologic intensive care. The primary goal of ICP management is to maintain ICP below 22 mmHg and cerebral pressure perfusion (CPP) above 60 mmHg. Optimization of oxygenation and cerebral blood flow (systolic blood pressure greater than 110 mm Hg) are essential. The use of positive end-expiratory pressure (PEEP) can increase intrathoracic pressure, thereby potentially increasing ICP by impeding venous drainage. Maintenance of euvolemia and strict monitoring of fluid balance are necessary. Several commonly described measures may be effective in reducing raised ICP such as keeping the patient’s head neutral and elevated at 15 to 30° as these optimize venous drainage. Proper muscle relaxation, adequate analgesia and sedation depth could further minimize elevation of ICP by reducing metabolic demand, ventilator asynchrony, venous congestion, and the sympathetic responses of hypertension and tachycardia. Fever increases brain metabolism and should be treated aggressively. Prophylactic antiepileptic medications should be considered only for traumatic brain injury. Dexamethasone and other steroids should not be used for treatment of IH, except in tumor patients. Hyperventilation should be limited to emergency management of life-threatening raised ICP until other methods of managing IH are available as it can acutely and reliably lower ICP and PaCO2. Hyperosmolar therapy is the principal medical management strategy for elevated ICP. Therapeutic strategies involve the use of mannitol or hypertonic saline. Mannitol is often considered the gold-standard therapy for medical management of IH but the preponderance of current evidence suggests that hypertonic saline could be. Failure of other conservative measures to control ICP should prompt consideration of the initiation of pentobarbital infusion. Aggressive strategies, like surgical decompression or hypothermia, carefully tested, have controversial effects on outcome. Decompressive craniectomy is indicated for massive ischemic stroke as it improved the survival rate and Glasgow outcome scale. Placement of an external ventricular drain should be considered in patients with moderately sized ventricles and signs and symptoms of raised ICP.

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Acute respiratory distress syndrome (ARDS) is an acute inflammatory lung injury, associated with increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue. There remains limited information about the epidemiology, recognition, management, and outcomes of patients with the ARDS, but in-hospital mortality is still high for those with moderate and severe ARDS (40.3% and 46.1%, respectively). Mechanical ventilation does not cure ARDS but simply buys time by maintaining a gas exchange sufficient for survival. The guiding principle of mechanical ventilation of ARDS is the new setting is less harmful to the lung structure than the previous one, thus avoiding the ventilator induced lung injury (VILI). Among outcome studies testing different tidal volumes, only the study comparing the two extreme values tested (6 mL/kg versus 12 mL/kg) showed a significant benefit of lower tidal volume. ‘The best positive end expiratory pressure (PEEP)’ does not exist. Recruitment maneuvers (RMs) are helpful in increasing aerated lung volume, which decreases strain and tidal recruitment/derecruitment. There is no definitive evidence regarding the clinical effectiveness of RMs to improve clinical outcomes of ARDS patients, although RMs may decrease the mortality of patients with ARDS without increasing the risk for major adverse events. There is no evidence for a difference between pressure control versus volume control ventilation in terms of physiological outcome or mortality. The effect of respiratory rate on the occurrence of VILI or outcome in ARDS has not been independently studied. Increasing inspiratory time has been suggested to improve oxygenation. Prone position (PP) is a standard practice in clinical treatment of ARDS patients to improve systemic oxygenation to any patient with moderate or severe ARDS as it may confer a statistically significant mortality advantage. There is evidence that neuromusculal blockade by cisatracurium besylate has an outcome benefit in ARDS patients since they improve lung mechanics and lung inflammation. Optimal dosing and monitoring strategies will need to be further studied.

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Cardiac surgery is a specialty with a relatively short history. The difficulties and particularities of Cardiac Surgery made apparent right from the beginning that there was a need forspecialized anesthesiological support. In 1940, Cardiac Surgeons pioneers recognized the role and contribution of cardiac anesthesiologists. In 1945, Blalock thanking his anesthesiologist co-workers Lamont and Harmel in public and mentioned that thanks to their anesthesiological support there “was no death during the first 55 operations”. Russell Brock, in 1949, highlighted the importance of collaboration between cardiac surgeons and cardiac anesthesiologists and mentioned “In this type of surgeries co-operation is necessary. The anesthesiologist plays a vital role and deserves special honor and recognition.” Since the first application of the electrocardiogram to operating theatres in 1950, the introduction of transesophageal echocardiography perioperatively in 1971, until the last decade with the application of coagulation monitoring, the newer data in the management of severe bleeding and the anesthesiological support in brand new minimal invasive techniques, cardiac anesthesiologists have vitally supported the evolution of cardiac surgery. The following text is a historical review describing the contribution of cardiac anesthesia in a continuing effort to improving clinical outcome and enhancing the safety of cardiac surgery.

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Invasive fungal infections are a growing problem in critically ill patients and are associated with increased morbidity and mortality. Complex medical and surgical problems, disruption of natural barriers, multiple invasive procedures and prolonged antibiotic treatment are some of the factors contributing to the alarming increase of fungal infections in the Intensive Care Unit (ICU) setting. In terms of occurrence rates, the most important fungal infections are invasive candidiasis (IC) and invasive pulmonary aspergillosis (IPA). Invasive candidiasis in ICU patients includes mainly candidemia, primary or catheter-related, and intra-abdominal candidiasis. Candida bloodstream infections occur at highest rates in the ICU population, with this setting accounting for 33–55% of all candidemias. The epidemiology of Candida infections is not constant.

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Το γαλακτικό οξύ παράγεται στο κυτταρόπλασμα από γλυκόλυση και μεταβολίζεται κυρίως από το ήπαρ (60%) (γλυκογονογένεση και νεογλυκογένεση) και από τα νεφρά (30%), τόσο στο φλοιό (τόπος μεταβολισμού)μέσω της νεογλυκογένεσης όσο και στο μυελό (τόπος παραγωγής). Η σχέση μεταξύ πυρουβικού και γαλακτικού οξέος είναι αμφίδρομη και το παραγόμενο γαλακτικό οξύ μπορεί να μετατραπεί είτε έμμεσα από το πυρουβικό σε οξαλικό οξύ και αλανίνη είτε άμεσα σε γλυκογόνο και γλυκόζη από τα περιπυλαία ηπατικά κύτταρα με τον κύκλο του Cori. Κατά συνέπεια, η αυξημένη γλυκόλυση οδηγεί σε αυξημένη παραγωγή γαλακτικού οξέος.

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After the implementation of Common Assessment Framework (CAF) – a useful quality tool – in the ICU of General Hospital of Trikala from 2012 up to 2015, we integrated the first cycle of self assessment and we present our results and conclusions of the past 3-year-period (2012- 2013 -2014). We analyzed CAF, FS- ICU 24, TISS-28 and Burn out syndrome questionnaires and medical indicators as Standardized mortality rate (SMR), Length of Stay (LOS), Standardized Resource Use (SRU), SMR/SRU, Therapeutic intervention scoring system (TISS-28), TISS-28/days of hospitalization, Nurse/Patient ratio, cost indicators and mortality. Analyzing the CAF questionnaire the score was 2.5-3.5, counting the indicator TISS-28 we found an average value higher than 50, concerning the burn-out syndrome questionnaire it was found that 58.82% of the respondent employees working in the ICU had mild symptoms of the syndrome. We analyzed the true Level of ICU (TISS-28/days of hospitalization) with the Level of ICU (nurse /patient ratio) and we found that they were not alike. We found an increase of mortality rate and LOS (length of stay) during the period of 2011 –2015 but a gradual reduction of the SMR/SRU indicator (the whole period ≤ 1) and a decline of the average cost/ patient and the average cost/ day of hospitalization.

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