2. Adverse Effects and Complications of Mechanical Ventilation
Dr.Sadr

3. 4 major concepts Know thy patient Know thy ventilator
Put the ventilator between you and the
patient
Alive ventilated patients

5. Interaction of factors linking difficult intubation to complications

6. Mechanical

7. Immediate complications of endotracheal intubation
Severe hypotension Severe hypoxia Esophageal intubation Intubation of RMB Dental injury Aspiration Pneumothorax Cardiac arrest Death

8. 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

9. Maxillary Sinus and Middle Ear Effusion
Maxillary effusion
Secondarily infected maxillary effusion
Middle ear effusion
Hearing impairment

10. Pharyngo-laryngeal Dysfunction
Post extubation discomfort
Hoarseness
Slowing of the reflex swallowing mechanism and risk of aspiration
Silent aspiration

11. Laryngeal Injuries
Erosive ulcers of vocal cords (posterior commissure)
Swelling and edema of the vocal cords
Granulomas

12. Tracheal Injuries
Cuff pressure tracheal damage: Tracheal ulceration edema
Sub mucosal hemorrhage
Tracheal dilatation
Tracheal stenosis

13. Esophagus, Stomach and Small Intestine

14. Upper gastrointestinal hemorrhage:
Stress
Decreased gastric mucosal protection secondary to a fall in splanchnic blood flow
Decreased motility of stomach and small intestine

15. Upper gastrointestinal hemorrhage:
Stress
Decreased gastric mucosa protection
secondary to a fall in splanchnic blood flow
Decreased motility of stomach and small intestine

16. 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

17. Large Bowel
Constipation
Abdominal distension

18. GI Effects of PPV

19. 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

20. Neurological Functions during Mechanical Ventilation
Decreased intracerebral blood volume
PEEP reduces cerebral perfusion pressure by decreasing venous return and increasing intracranial pressure
Disrupt Sleep

21. Mechanisms by which mechanical Ventilation Disrupt Sleep

22. 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

23. Ventilation complications Mode specific

25. Ventilator-associated Pneumonia
Definition of VAP
The development of a new pneumonia at least 48 hrs after initiation of mechanical ventilation

26. Independent risk factors for the development of VAP in children
Immunodeficiency
Immunosuppression
Neuromuscular blockade

27. 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 H2-receptor-blocker therapy
reintubation
transport out of the ICU while intubated
nasoenteric tube
in-line nebulizers
manipulation of ventilator circuits

28. Cumulative risk of developing VAP with the duration of mechanical ventilation.

29. 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.

30. 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%)

31. 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.

32. 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.

33. 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.

34. Diagnosis of VAP in children
clinical & without the use of bronchoscopy

36. 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.

37. 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

39. 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.

40. Proposed bundle for prevention of ventilator- associated pneumonia in infants and children
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   
Oral rinsing/cleaning with chlorhexidine (0.12%)  
Use of toothbrush and oral swabs in daily oral care

42. 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.

43. Ventilator-associated Lung Injury (VALI)
Definition: lung damage caused by application of positive or negative pressure to the lung by mechanical ventilation.
oxygen toxicity

44. Mechanisms of VALI
Volutrauma: damage caused by over-distension. High volume or high-end inspiratory volume injury
Barotrauma: high pressure induced lung damage
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

45. Mechanisms of VALI
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
The pressure needed to reopen an occluded airway is inversely proportional to its diameter → damage occurs distally

46. Mechanisms of VALI
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

47. Oxygen toxicity
FiO2 > 60% for more than 72 hours
Elevated intrathoracic pressures with decreased venous return, intravascular volume repletion

50. Thanks you …