Presentation on theme: "1. Adverse Effects and Complications of Mechanical Ventilation Dr.Sadr."— Presentation transcript:
Adverse Effects and Complications of Mechanical Ventilation Dr.Sadr
4 major concepts Know thy patient Know thy ventilator Put the ventilator between you and the patient Alive ventilated patients
Interaction of factors linking difficult intubation to complications
Immediate complications of endotracheal intubation Severe hypotension Severe hypoxia Esophageal intubation Intubation of RMB Dental injury Aspiration Pneumothorax Cardiac arrest Death
Injuries to Face, Lips and Oropharynx Trauma to the lip and cheeks from the tube tie Perioral herpes Injuries to the tongue particularly when entrapped between the endotracheal tube and the lower teeth Pressure ulcers to the palate and oropharynx are very uncommon
Upper gastrointestinal hemorrhage: Stress Decreased gastric mucosal protection secondary to a fall in splanchnic blood flow Decreased motility of stomach and small intestine
Upper gastrointestinal hemorrhage: Stress Decreased gastric mucosa protection secondary to a fall in splanchnic blood flow Decreased motility of stomach and small intestine
Liver and Gallbladder Reduction in portal venous flow secondary to the fall in cardiac output Hepatic engorgement Elevation of serum transaminases and hyperbilirubinemia Reduction in drug clearance secondary to reduction of hepatic blood flow
Large Bowel Constipation Abdominal distension
GI Effects of PPV
Renal Effects of MV The usual renal response to reduction of cardiac output and mean arterial pressure Reduction in urine output secondary to a fall in the trans mural pressure of the right atrium that results in reduction of the secretion of atrial naturitic peptide and the activation of renin-angiotensin-aldosterone system and pituitary vasopressin secretion
Neurological Functions during Mechanical Ventilation Decreased intracerebral blood volume PEEP reduces cerebral perfusion pressure by decreasing venous return and increasing intracranial pressure Disrupt Sleep
Mechanisms by which mechanical Ventilation Disrupt Sleep
Asynchrony with the ventilator Fighting the ventilators Inconsistent tidal volume Increase work of breathing Barotraumas and thoracic air leak Insufficient gas exchange Disturbances in the cerebral blood flow
Ventilation complications Mode specific
Definition of VAP The development of a new pneumonia at least 48 hrs after initiation of mechanical ventilation Ventilator-associated Pneumonia
Independent risk factors for the development of VAP in children Immunodeficiency Immunosuppression Neuromuscular blockade
Additional risk factors genetic syndromes with neuromuscular weakness burns steroid administration use of total parenteral nutrition antibiotic use longer ICU lengths of stay use of indwelling catheters use of H 2 -receptor-blocker therapy reintubation transport out of the ICU while intubated nasoenteric tube in-line nebulizers manipulation of ventilator circuits
Cumulative risk of developing VAP with the duration of mechanical ventilation.
Although length of time with an endotracheal tube in place increases the risk of nosocomial pneumonia, the greatest risk is during the first 2 weeks of intubation. Nearly all intubated children will have colonization of their endotracheal tube with hospital-acquired organisms by a mean of 5 days.
The most common organisms isolated in the developing countries Enterobacteriaceae spp. (26%) Pseudomonas aeruginosa (26%), with 60% resistant to fluoroquinolones S. aureus (22%), with 84% methicillin resistant Acinetobacter spp. (20%)
The bacterial organisms identified most often are gram-negative bacilli, with P. aeruginosa being the most common species identified in PICUs. The second most common bacterial etiology of pediatric nosocomial pneumonia is the gram-positive organisms. The frequently isolated bacteria are S. aureus and coagulase- negative staphylococci.
S. epidermidis nosocomial pneumonia is a common cause in the NICU population and is typically the result of hematogenous spread. Anaerobic nosocomial pneumonia is rare in the pediatric population but accounts for 23% of nosocomial pneumonias in adults.
Viruses, predominantly RSV common cause of nosocomial respiratory infections. Fungal infections are exceedingly rare but may occur in children who are immunosuppressed, especially if they frequently receive broad-spectrum antibiotics.
Diagnosis of VAP in children clinical & without the use of bronchoscopy
The CDC criteria for diagnosis of VAP in infants and children are evidence of new or progressive infiltrate, fever or leukopenia with new onset of purulent sputum, and increased sputum production.
Recognized methods to determine the causative organism positive blood cultures that cannot be attributed to another source, positive cultures from pleural fluid, a positive bronchoalveolar lavage specimen despite its limitations, >5% of cells from bronchoalveolar lavage containing intracellular bacteria, a positive culture of lung parenchyma, histopathologic evidence of fungal hyphae
Once nosocomial pneumonia is suspected, empiric treatment should be started, covering the most likely organisms with consideration of the hospital's resistance patterns. When a specific causative is identified, antibiotic coverage should be adjusted. If the diagnostic workup is negative and a viral etiology is suspected, the discontinuation of antibiotics may be considered.
Items to prevent iatrogenic spread of infection Adherence to good hand hygiene practices Use of universal precautions Use of appropriate isolation techniques based on infectious organism (proven or suspected) Items to prevent aspiration of gastric contents Elevate the head of the bed between 30 and 45 degrees Monitor/drain gastric contents Items to improve oral hygiene o Oral rinsing/cleaning with chlorhexidine (0.12%) o Use of toothbrush and oral swabs in daily oral care Proposed bundle for prevention of ventilator- associated pneumonia in infants and children
Endotracheal Suctioning? Endotracheal suctioning should not be a routine intervention, but it should be performed when obstructive secretions are indicated by clinical assessment of a patient’s respiratory status. The instillation of physiological saline should not be a routine part of endotracheal suctioning.
Ventilator-associated Lung Injury (VALI) Definition: lung damage caused by application of positive or negative pressure to the lung by mechanical ventilation. oxygen toxicity
Mechanisms of VALI Volutrauma: damage caused by over- distension. High volume or high-end inspiratory volume injury Volutrauma: damage caused by over- distension. High volume or high-end inspiratory volume injury Barotrauma: high pressure induced lung damage Barotrauma: high pressure induced lung damage Similar histological appearance, high- permeability pulmonary edema in uninjured lung & exacerbated damage in injured lung Similar histological appearance, high- permeability pulmonary edema in uninjured lung & exacerbated damage in injured lung Alveolar over-distention rather than pressure itself causes lung injury Alveolar over-distention rather than pressure itself causes lung injury
Mechanisms of VALI Atelectotrauma: lung injury associated with repeated recruitment and collapse, low end- expiratory volume injury Atelectotrauma: lung injury associated with repeated recruitment and collapse, low end- expiratory volume injury Theoretically prevented by using a level of positive end-expiratory pressure (PEEP) greater than the lower inflection point of the pressure volume curve Theoretically prevented by using a level of positive end-expiratory pressure (PEEP) greater than the lower inflection point of the pressure volume curve The pressure needed to reopen an occluded airway is inversely proportional to its diameter → damage occurs distally The pressure needed to reopen an occluded airway is inversely proportional to its diameter → damage occurs distally
Biotrauma: pulmonary and systemic inflammation caused by the release of mediators from lungs subjected to injurious mechanical ventilation Biotrauma: pulmonary and systemic inflammation caused by the release of mediators from lungs subjected to injurious mechanical ventilation Protective ventilation can lower concentration of cytokines in lung and plasma Protective ventilation can lower concentration of cytokines in lung and plasma Mechanisms of VALI
Oxygen toxicity FiO 2 > 60% for more than 72 hours Elevated intrathoracic pressures with decreased venous return, intravascular volume repletion