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PNEUMONIA

The incidence of postoperative pneumonia varies depending on risk factors, ranging


from an incidence of 1.5% to as high as 15.3% in high-risk groups.
The 30-day postoperative mortality for all groups can be as high as 21%, depending on the severity of
illness, comorbidities, and causative pathogens.26,27
Data available in the American College of Surgeons NSQIP program (20052008), from patient who went
colectomy, postoperative pneumonia was significantly more common in patients undergoing emergent compared
with elective surgery (11.1% vs 2.9%)

FURTHER CATEGORIZATION FOR PNEUMONIA
Guidelines from American Thoracic Society (ATS)/Infectious Diseases Society of America (IDSA) in 2005

Hospital acquired pneumonia (HAP)
Ventilator-associated pneumonia (VAP)
Health careassociated pneumonia (HCAP)

PATHOPHYSIOLOGY

Under normal circumstances, the lower respiratory tract is sterile.
Both HAP and VAP are generally associated with introduction of bacteria to the sterile lower respiratory
tract; this can be exacerbated by impaired host defenses.

The introduction of bacteria to the lower airways occurs through 2 important mechanisms:
bacterial colonization of the aerodigestive tract
aspiration of contaminated secretions into the lower airway.

Several factors promote these mechanisms, including the presence of invasive devices, medications altering
gastric emptying and pH, contaminated water, medications, and respiratory therapy equipment.

In VAP, the colonization pathway occurs according to the steps illustrated in FIG 1.


DEFINITIONS

HAP is defined as pneumonia occurring more than 48 hours after hospital admission.

VAP is a type of HAP that develops more than 48 hours after endotracheal intubation.

HCAP is pneumonia that occurs in a patient with health care contact as defined by 1 or more of the following
criteria:
a patient hospitalized for 2 days or more in an acute care facility within 90 days of infection;
a patient residing in a nursing home or long-term care facility;
a patient who has attended a hospital or hemodialysis center;
a patient who has received intravenous antibiotic therapy, chemotherapy, or wound care within 30 days of the
current infection;
any patient who is a family member of a patient with a multidrugresistant
(MDR) pathogen.

DIAGNOSIS

Pneumonia should be suspected in a patient with new or progressive infiltrate on chest
radiographs as well as clinical characteristics such as fever, purulent sputum, leukocytosis, and hypoxia.

When findings at autopsy are used as a reference, the combination of radiographic infiltrate plus 2 of 3 clinical
features (fever >38_C, leukocytosis/
leukopenia, purulent secretions) resulted in 69% sensitivity and 75% specificity for
pneumonia

The diagnosis of VAPis suspected when a patient on mechanical ventilation develops
new pulmonary infiltrate with fever, leukocytosis, and purulent secretions.

At present, the Centers for Disease Control and Prevention (CDC) define VAP using
a combination of radiologic, clinical, and laboratory criteria, in patients who are ventilated for longer than 48
hours.

Pneumonia is classified into 3 types as illustrated in Fig. 3. These types are clinically defined (PNEU-1), common
bacterial, fungal, or atypical pneumonia (PNEU-2), and pneumonia in immunocompromised patients (PNEU-3).
The diagnosis requires new or progressive and persistent infiltrate/consolidation/cavitation
on 2 or more serial chest radiographs
.


To avoid inadequate antibiotic therapy, early use of empiric broad-spectrum antibiotics
to cover all potential causative pathogens is required. The choice of empiric antibiotics
in pneumonia should be based on national guidelines with knowledge of the
most common pathogens, and also with consideration of local antibiograms, particularly
in surgical ICUs
It is crucial to start antibiotics when a clinical diagnosis is made,
immediately after cultures are obtained. To avoid excessive antibiotics, therapy
should be modified to a narrower spectrum (de-escalation) as soon as culture results
and antimicrobial susceptibilities are available


HAP PREVENTION

Some institutions have initiated aggressive HAP prevention efforts in surgical patients
to reduce postoperative pneumonia.70 The program consisted of education of physicians
and staff and a standardized postoperative electronic order set consisting of
incentive spirometer, chlorhexidine oral hygiene, early ambulation, and head-of-bed
elevation. This strategy was associated with an 81% decrease in postoperative pneumonia
from 2006 to 2008.

VAP PREVENTION

The strategies to prevent infection are therefore aimed at (1) reducing bacterial colonization and (2)
decreasing the incidence of aspiration.

Decreased incidence of aspiration can beachieved through improved positioning, increased head-of-bed
elevation, and use of specialty endotracheal tubes that aspirate subglottic secretions.

Bacterial colonization can be reduced by minimizing the days on mechanical ventilation through weaning
protocols, use of chlorhexidine in the posterior pharynx, and silver-coated endotracheal tubes.



ACUTE RESPIRATORY FAILURE


Acute respiratory failure in the postoperative setting can be caused by loss of airway
protection, failure to oxygenate (hypoxemic respiratory failure, type 1), or failure to
ventilate (hypercapnia respiratory failure, type 2)

(GAMBAR)


Hypoxic respiratory failure (type 1) is defined by a PaO2 of less than 60 mm Hg (not taking into account chronic
illness).
Hypocapnia can often accompany hypoxia because of increased ventilatory drive.

This type of respiratory failure is more common,and usually the underlying problem is at the pulmonary
capillary/alveolar interface.
Virtually all processes in type 1 respiratory failure involve either fluid filling or collapse of alveolar units.

These injuries are usually categorized into diffusion defects or ventilation-perfusion mismatch.




Hypercapneic respiratory failure (type 2) is defined by a PaCO2 of greater than 50mm
Hg (not taking into account chronic illness).

Hypoxemia can be common in these patients, because increased alveolar CO2 can displace alveolar O2. When
looking for the underlying cause in type 2 respiratory failure, it is best to proceed in a systematic
manner from the brain to the lung.

A central loss of ventilation can be due to sedation, narcotic overdose, stroke, or medication. Spinal cord
procedures or traumatic injuries can result in loss of diaphragm or accessory muscle use. Trauma causing
mechanical injury to the chest can cause broken ribs, flail chest, pneumothorax, hemothorax, or pleural effusions
that make ventilation difficult.

For most postoperative surgical patients with severe acute respiratory failure, either
hypoxemic or hypercapneic, early intubation and initiation of mechanical ventilation
should be considered. A brief period of noninvasive ventilation is generally considered
if there is a promptly reversible cause of the acute respiratory failure (ie, atelectasis or
pulmonary edema). All patients with signs and symptoms of acute respiratory failure
must be monitored and treated in an ICU.


SUMMARY
The incidence of postoperative pulmonary complications, particularly postoperative
pneumonia and acute respiratory failure, is a significant cause of morbidity and
mortality. The clinical diagnosis of pneumonia can be challenging. However, when
pneumonia is suspected, it is important first to obtain lower respiratory tract samples
for culture. With high clinical suspicion for pneumonia, it is crucial to begin early appropriate
empiric antimicrobial therapy to cover all potential causative pathogens. Attention
must be paid to the possibility of HCAP and propensity of MDR bacterial
pneumonia in high-risk groups. Antibiotics must be tailored to the patient with consideration
of both local microbiology and data from national guidelines. National rates
of VAP remain highest in surgical, trauma, and burn ICUs. Prevention of VAP can be
optimized by reducing the risk of aspiration and bacterial colonization of the airway
through evidence-based preventive strategies (chlorhexidine, semirecumbent position,
CASS or silver-coated endotracheal tubes, spontaneous awakening and
breathing trials, and ventilator-weaning protocols).

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