الفهرس 
Review of LiteratureOnly 14 pages are availabe for public view
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Abstract
T
he diaphragm is the most important respiratory muscle that plays a crucial role in maintaining normal breathing pattern especially in critically ill patients. It is markedly affected in mechanically ventilated patients and predispose to prolonged ICU stay. This dysfunction if predominantly caused by ventilation is called ventilator induced diaphragmatic dysfunction (VIDD). Most studies show that VIDD occurs in a progressive, time-dependent manner, although its degree is influenced by different MV modes and other clinical variables. VIDD has a pathophysiology similar to ventilator-induced lung injury (VILI), which is characterized by diffuse inflammation and increased oxidative stress, ultimately leading to impaired gas exchange. However, the mechanism underlying VIDD potentially involves a multistep process including oxidative stress, muscle weakness, structural damage and myofiber remodeling.. Therefore, a detailed knowledge of the molecular mechanisms underlying VIDD is crucial for designing potential strategies and reducing prolonged MV use, ICU stay and eventually ICU mortality.
Many diagnostic approaches were implemented targeting early detection of VIDD. Tests of the respiratory muscles are the most important approach especially ultrasonagraphic measurements because the ultrasound (US) is portable, ubiquitous in medical facilities, has no risk of ionizing radiation, allows visualization of structures below and above the diaphragm, gives functional information about the muscle itself and can be repeated if follow up is required. It carries the advantage of assessing both the structural and functional components of the diaphragm at the bedside.
Preventing diaphragm myotrauma during ventilation is now recognized as a pressing priority for the field of MV, with the potential to substantially improve outcomes for patients. Because diaphragm dysfunction commences within mere hours of initiating ventilation, early intervention is required to protect the diaphragm. The approach is to maintain an appropriate level of inspiratory diaphragmatic effort while avoiding potentially injurious forms of patient–ventilator dyssynchrony. Prolonged periods of complete diaphragmatic rest should be avoided and diaphragmatic contraction preserved whenever possible, Respiratory muscle training may lead to improved weaning success. Treatment of any reversible causes of diaphragmatic weakness should be treated promptly to enhance the improvement of diaphragmatic function. There is also a pharmacological and non-pharmacological alternatives proved to promote diaphragmatic efficiency.
The use of US as a monitor for the diaphragm’s dynamic function in terms of Diaphragmatic Excursion (DE) and structure in terms of Diaphragmatic Thickness Fraction (DTF) showed promising results. DE is the difference in the diaphragmatic position during inspiration and expiration and it was measured during the patients’ spontaneous breathing trials. The diaphragmatic thickness is measured by M-mode in the zone of apposition between the two layers of the pleura and the peritoneum. Diaphragmatic thickness has been previously correlated with the strength of the diaphragm, but not the fatigability. The DTF is an indicator of the work of breathing. DTF was found to be more accurate than diaphragmatic thickness because it abolished the effect of body weight and height on diaphragmatic thickness. A DTF of less than 20% or a tidal excursion of less than 10 mm were used as cutoff parameters to identify diaphragmatic dysfunction.
Our study was conducted on 60 mechanically ventilated patients due to cerebral insult. Each patient was subjected to a pressure-targeted mode of ventilation appropriate to his respiratory pattern achieving the unison between the patient and ventilator guided by pulse oximetry and ABG analysis. The value of DE was highest in the PSV group in our study, reflecting enhanced diaphragmatic function and a better outcome in terms of the ICU stay. The DE was lowest in the SIMV group, which signifies the effect of increased work of breathing on diaphragmatic function.
However, there was no statistically significant difference in DTF between the four groups. On the other hand, there was a statistically significant difference between T1, T2, and T3 in each group. We assumed that increasing the duration of ventilation caused diaphragmatic thinning and a decrease in DTF, resulting in DD. PSV was found to be the best mode with the least risk of DD when compared with other pressure-targeted modes of ventilation.
CONCLUSION
T
he US is crucial in the assessment of diaphragmatic function at a point in time or over time and in comparison of different modes of ventilation regarding DD, the incidence of DD in patients with cerebral insult decreased with the decrease in ventilatory support. PSV was found to be the best mode with the least risk of DD when compared with other pressure-targeted modes of ventilation.