Η οξεία εγκεφαλική βλάβη (acute brain injury, ABI) αποτελεί συχνό κλινικό πρόβλημα, που απαιτεί άμεση και επείγουσα αντιμετώπιση. Περιλαμβάνει οποιαδήποτε πάθηση επηρεάζει οξέως το κεντρικό νευρικό σύστημα (ΚΝΣ), [π.χ. τραυματική εγκεφαλική βλάβη (traumatic brain injury, TBI)] και έχει δύο συστατικά, την πρωτογενή (primary brain injury, PBI) και τη δευτερογενή εγκεφαλική βλάβη (secondary brain injury, SBI)1. Continue reading

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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