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M.Jeschke - Handbook of Burns Volume 1 Acute Burn Care - 2013.pdf
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R. Cartotto

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Fig. 3. (a) Pressure Vs time tracing during HFPV [50], (b) comparison of pressure Vs time tracings for CMV and HFOV [79], (c) pressure Vs time tracing during APRV [80]

smoke inhalation suggests that APRV compared favourably to HFPV by improving oxygenation at lower airway pressures than HFPV [82].

Ventilator associated pneumonia (VAP)

Ventilator Associated Pneumonia (VAP) is the most common infection occurring in critically ill patients who receive mechanical ventilation. Burn patients are particularly predisposed to VAP due to the combined effects of prolonged intubation and ventilation, burn-related immunosupression, inhalation injury, and prolonged length of stay in the burn intensive care setting. Estimates of the incidence of VAP in burn patients range between 22 to 26 cases per 1000 ventilator days [84, 85].

The most widely accepted mechanism of VAP involves microbial colonization of the oropharynx and stomach which, when followed by chronic microaspiration of secretions part the endotracheal tube balloon cuff, leads to contamination of the usually sterile lower respiratory tract. The presence of an endotracheal tube impairs many of the normal defenses that would protect the lower airways, including the usual glottic barrier, mucociliary clearance and the ability to cough and effectively clear secretions [86, 87]. Early VAP (ie within four days of intubation) most commonly involves organisms such as

Streptococcus pneumonia and Haemophilus influenzae while gram-negative bacilli such as Pseudomonas aeruginosa, E Coli, and Acinetobacter, along with methacillin-resistant Staphylococcus aureus predominate later on [87]. In burn units, Acinetobacter baumannii has become particularly widespread pathogen, and frequently is multi-drug resistant[88].

Diagnosis of VAP in a mechanically ventilated burn patient may be difficult due to the presence of overlapping systemic inflammation, pulmonary edema, and ALI or ARDS. There is no consensus on a set of guidelines by which to diagnose VAP in burn patients. VAP should be suspected when findings of fever, increasing or purulent sputum production, leukocytosis or leucopenia, and worsening infiltrates on the chest radiograph, are present. Quantitative bacteriologic cultures obtained using brocheocalveolar lavage (BAL) probably represent a preferable approach over simple endotracheal suction aspirates. The threshold for a positive quantitative culture remains controversial and ranges between 103 –105 cfu/mL [88, 89].

A recent set of practice guidelines for the prevention and treatment of VAP in the burn patient, pub-

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