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
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).