Transcript Adverse Effects and Complications of Mechanical Ventilation

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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
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Mechanical
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
Maxillary Sinus and Middle Ear
Effusion
• Maxillary effusion
• Secondarily infected maxillary effusion
• Middle ear effusion
• Hearing impairment
Pharyngo-laryngeal Dysfunction
• Post extubation discomfort
• Hoarseness
• Slowing of the reflex swallowing
mechanism and risk of aspiration
• Silent aspiration
Laryngeal Injuries
• Erosive ulcers of vocal cords (posterior
commissure)
• Swelling and edema of the vocal cords
• Granulomas
Tracheal Injuries
Cuff pressure tracheal damage:
Tracheal ulceration edema
Sub mucosal hemorrhage
Tracheal dilatation
 Tracheal stenosis
Esophagus, Stomach and Small
Intestine
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
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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
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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
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Ventilator-associated Pneumonia
• Definition of VAP
The development of a new pneumonia
at least 48 hrs after initiation of
mechanical ventilation
Independent risk factors for the
development of VAP in children
Immunodeficiency
Immunosuppression
Neuromuscular
blockade
Additional risk factors
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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
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 coagulasenegative 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.
Proposed bundle for prevention of ventilatorassociated pneumonia in infants and children
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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
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
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Volutrauma: damage caused by overdistension. High volume or high-end inspiratory
volume injury
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Barotrauma: high pressure induced lung
damage
Similar histological appearance, highpermeability pulmonary edema in uninjured
lung & exacerbated damage in injured lung
Alveolar over-distention rather than pressure
itself causes lung injury
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Mechanisms of VALI
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Atelectotrauma: lung injury associated with
repeated recruitment and collapse, low endexpiratory volume injury
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Theoretically prevented by using a level of positive
end-expiratory pressure (PEEP) greater than the
lower inflection point of the pressure volume curve
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The pressure needed to reopen an occluded
airway is inversely proportional to its diameter →
damage occurs distally
Mechanisms of VALI
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Biotrauma: pulmonary and systemic
inflammation caused by the release of
mediators from lungs subjected to injurious
mechanical ventilation
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Protective ventilation can lower
concentration of cytokines in lung and
plasma
• Oxygen toxicity
FiO2 > 60% for more than 72 hours
Elevated intrathoracic pressures with
decreased venous return, intravascular
volume repletion
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