**Part 5**

**Cardiothoracic Anaesthesia** 

318 Front Lines of Thoracic Surgery

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[32] Kalfa N, Allal H, Raux O, Lopez M, Forgues D, Guibal MP et al. Tolerance of laparoscopy and thoracoscopy in neonates. *Pediatrics* 2005; 116(6):e785-e791. [33] Klarenbeek BR, Bergamaschi R, Veenhof AA, van der Peet DL, van den Broek WT, de

[34] Eshuis EJ, Slors JF, Stokkers PC, Sprangers MA, Ubbink DT, Cuesta MA et al. Long-term

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[38] Bal S, Elshershari H, Celiker R, Celiker A. Thoracic sequels after thoracotomies in children with congenital cardiac disease. *Cardiol Young* 2003; 13(3):264-267. [39] Jaureguizar E, Vazquez J, Murcia J, Diez Pardo JA. Morbid musculoskeletal sequelae of thoracotomy for tracheoesophageal fistula. *J Pediatr Surg* 1985; 20(5):511-514.

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**18** 

**Ventilator-Induced Lung Injury: Mechanisms** 

**and Future Therapeutic Interventions** 

*1Laboratory of Experimental Intensive Care and Anesthesiology (LEICA),* 

*2Department of Intensive Care Medicine, Academic Medical Center, Amsterdam,* 

*4Laboratory of Neuroimmunology and Developmental Origins of Disease (NIDOD),* 

Mechanical ventilation has become a standard technique to support the life of the critically ill patient in the intensive care unit (ICU) (Tobin, 2001). In general, mechanical ventilation is applied when the patient's spontaneous ventilation is inadequate to maintain life. Especially patients who have developed acute respiratory failure require mechanical ventilation (Slutsky, 1993). Patients diagnosed with acute lung injury (ALI) suffer from severe pulmonary dysfunction which may persist for a long period of time. The extent and severity of ALI differs among patients, with the acute respiratory distress syndrome (ARDS) being the most severe manifestation of this lung disease (Schwarz, 2001). ALI and ARDS are characterized by the acute onset of diffuse neutrophilic alveolar infiltrates, protein-rich edema due to enhanced alveolar-capillary permeability and hypoxemic respiratory failure (ratio of arterial oxygen partial pressure to fractional inspired oxygen concentration, PaO2/FiO2 < 300 for ALI or < 200 for ARDS) (Ashbaugh et al, 1967; Petty & Ashbaugh, 1971). These pulmonary disorders may result from local injuries like pneumonia, gastric aspiration, near-drowning and lung contusion, but also from systemic events like severe

sepsis, shock and blood transfusions (Hudson et al, 1995; Ware & Matthay, 2000).

chapter will primarily focus on experimental findings, the term VILI will be used.

**2. Pathogenesis of ventilator-induced lung injury** 

similar to those seen in ALI and ARDS (Tsuno et al, 1991).

Although mechanical ventilation is a life-saving procedure, it has the potential to cause damage in healthy lung tissue or aggravate damage in diseased lung tissue (Dreyfuss & Saumon, 1998; Slutsky, 1999). The pulmonary complications secondary to mechanical ventilation are frequently referred to as ventilator-associated lung injury (VALI) in the clinical setting and ventilator-induced lung injury (VILI) in the experimental setting. As this

VILI is characterized by enhanced alveolar-capillary permeability, accumulation of proteinrich lung edema, disturbed alveolar fibrin turnover, production of inflammatory mediators, and - ultimately - impaired gas exchange. Interestingly, these patterns of injury are very

**1. Introduction** 

Maria A. Hegeman1,2, Marcus J. Schultz1,2, Adrianus J. van Vught3 and Cobi J. Heijnen4

*3Department of Pediatric Intensive Care,* 

*The Netherlands* 

*University Medical Center Utrecht, Utrecht,* 
