Chapter 8

Introduction

About 10% of CAP patients require ICU admission because of development of hypoxemic respiratory failure or systemic signs of sepsis. In only about 25% of these cases the pathogen is identified on admission to the ICU leading to delayed specific therapy with increased complications and mortality.1 HCAP runs a worse clinical course because of multi drug resistant (MDR) organisms and coexistent morbidities with an overall mortality of 25% which is even higher if associated with Adult Respiratory Distress Syndrome (ARDS).

Classification

The most common classification is based on the origin of the pneumonia — CAP or HCAP. The pathogens involved in these two are different with different drug susceptibility profiles. CAP is associated with easily identified and treatable pathogens, while HCAP is associated with MDR pathogens especially when hospital stay is prolonged (see Table 1 for identification of the common pathogens in these two categories).

Table 1. Classification of pneumonia by its origin and most common pathogens in each of them.

In one observational study, the most common pathogens associated with CAP admitted to ICU are Streptococcus pneumoniae, Staphylococcus aureus and Pseudomanas aeruginosa.2 Legionella pneumophila is one of the atypical pathogens that can cause severe CAP that is associated with immune-mediated extrapulmonary symptoms.¹ Staphylococcus aureus is also a causative organism that can cause severe CAP with a growing number being methicillin-resistant (MRSA).¹

In immunocompromised patients (e.g., Human immunodeficiency Virus (HIV)), opportunistic pathogens like Herpes viruses, Aspergillus species, Pneumococcus jiroveci and Cryptococcus neoformans may be involved. Antimicrobial therapy should be directed at these organisms when suspected or identified.

In another observational study, the most common pathogens associated with HCAP were MRSA and Pseudomonas aeroginosa.³ Because of their associated morbidity and mortality, every effort should be made to establish an early microbiological diagnosis including drug sensitivity.

Diagnosis and Microbiology

Once the diagnosis of pneumonia is considered, cultures from the blood as well as the sputum should be obtained before starting the antibiotics. The risk of bacteremia is dependent on multiple factors. A prediction score has been suggested and evaluated in a retrospective study involving 1,136 patients. The overall rate of bacteremia was between 12–16%. The score consisted of 6 variables: liver disease, pleuritic pain, tachycardia, tachypnea, systolic hypotension, and absence of prior antibiotic treatment. With a score of 1, the risk of bacteremia was < 8%, while a score of 2, the risk of bacteremia was between 14–63%.⁴

Urine should be sent for Antigen assays for S. pneumoniae and L. pneumophila. For Legionella, urinary antigen assay has a sensitivity of 74% and specificity of 99%, while the pneumococcal antigen assay has a sensitivity of 71% and specificity of 96%.

In non-intubated patients, the reliability of sputum obtained from deep coughing is unknown. In those patients, awake Fiberoptic Bronchoscopy (FOB) and Bronchoalveolar Lavage (BAL) may be employed to obtain sputum samples. In intubated patients, multiple techniques are available including Protected Specimen Brushing (PSB), FOB with BAL and miniBAL (without FOB). Diagnostic accuracy is similar with each of these techniques. Their use is largely dependent on resources and center experience. Quantitative cultures may differentiate true infection from contaminants in the respiratory tract. Most of the literature is extrapolated from studies done on VAP.⁵

Polymerase Chain Reaction (PCR) is being used increasingly as a diagnostic technique. Its advantages include rapidity, sensitivity, and detection of both bacterial and viral pathogens. It has also some limitations including cost and inability to differentiate between colonizations from true infections.1 In immunocompromised patients, BAL samples should be sent for fungal antigens. PCR assays also may have some role in this patient population.¹

Treatment

Recommended criteria for ICU admission are shown in Table 2. The presence of one major criterion is an indication for ICU. The presence of ≥ 3 minor criteria is an indication for admission to high-level monitoring settings (e.g., level II bed).⁶

Once the diagnosis is suspected, early initiation of antimicrobial therapy is very important since it is associated with better outcome. This is especially important in patients with severe sepsis or septic shock. A summary of antibiotic regimens recommended for both severe CAP and HCAP is shown in Table 3. For severe CAP in the ICU, combination therapy is recommended to cover the most common pathogens and is superior to monotherapy.⁶ This should consist of a β-lactam plus a macrolide or a fluoroquinolone. Antipseudomonal coverage is only required if there are risk factors for Pseudomonal infections, such as structural lung disease, bronchiectasis, repeated exacerbations of Chronic Obstructive Pulmonary Disease (COPD) with frequent steroid and/or antibiotic administration, and prior antibiotic use.⁶ If there are risk factors for MRSA; such as end-stage renal disease, injection drug abuse, and prior antibiotic use, addition of linezolid or vancomycin is recommended.⁶

Table 2. Major and minor criteria for ICU admission.

Table 3. Recommended empiric antibiotic therapy.

In HCAP, the antibiotic choice will depend on the risk of MDR pathogens. “Early-onset” HCAP patients (within four days of the index admission) usually have low risk. “Late-onset” HCAP that occurs after five days and early onset with recent hospitalization or coming from a health-care facility (nursing home, dialysis center) usually have a high risk of MDR pathogens.7 Those should be treated with triple therapy to cover for Pseudomonas species, MDR gram negatives, and MRSA until cultures are available.⁷

After 48–72 hours, checking the cultures and reassessment of the clinical response are required. If the patient has a good clinical response and a causative pathogen is identified, de-escalation of the antibiotics according to the cultures and sensitivity is recommended. Consideration should be given to stopping the antibiotics if all reliable cultures from the respiratory tract are negative. If the patient is not improving and organisms identified, adjustment of the antibiotics obviously is required. If cultures are still negative by that time, consider complications (e.g., empyema) or other diagnoses. All patients should receive intravenous antibiotics initially. Switching to oral/enteral route is reasonable in patients with good clinical response. Combination therapy is recommended in all patients with high risk of MDR organisms. Monotherapy is acceptable in the absence of resistant organisms. Total duration of directed therapy is 7–8 days and there is no benefit from longer courses.⁷

Management of Organ Failure

The two most common indications for an ICU admission in patients with severe pneumonia are septic shock and respiratory failure. Severe sepsis and septic shock should be managed according to the guidelines in Surviving Sepsis Campaign. The first bundle, which should be completed within three hours, includes measuring serum lactate, obtaining blood cultures, administering broad-spectrum antibiotics, and fluid resuscitation. The second bundle, which should be completed within six hours, includes starting vasopressors (for persistent hypotension), measuring central venous pressure (CVP) and central venous oxygen saturation (ScvO₂) and remeasuring lactate if initially elevated. End points of resuscitation are CVP ≥ 8 mmHg, central venous oxygen saturation ≥ 70% and normalization of lactate.⁸

Hypoxemic and/or hypercapnic respiratory failure can be managed initially by a trial of Non-Invasive Ventilation (NIV). Contraindications for NIV include decreased level of consciousness, hemodynamic instability, inability to protect the airway or clear secretions, severe gastrointestinal bleeding and inability to fit the mask, or undrained pneumothorax.1 Failure of NIV and/or clinical criteria of ARDS (acute onset, Partial Pressure of Arterial Oxygen/Fraction of Inspired Oxygen (PaO₂/FiO₂) ratio < 300, bilateral pulmonary infiltrates with normal left ventricular function) are indications for intubation and mechanical ventilation.¹ Management of hypoxemia in ARDS is beyond the scope of this chapter.

VAP

VAP is traditionally defined as a hospital-acquired pneumonia that develops in patients who have been mechanically ventilated for ≥48 hours. It is subclassified into early onset and late onset. Early onset VAP usually develops within four days of mechanical ventilation, while late onset develops after four days. Early onset is usually caused by antibiotic-susceptible organisms and late-onset by MDR organisms.⁹

VAP is the most common nosocomial infection that develops in mechanically ventilated patients. Its incidence has been estimated as 9–27% of mechanically ventilated patients, with about five cases per 1,000 ventilator days. VAP has been a significant hospital burden due to increased ICU and hospital mortality, with an estimated attributable mortality of 9%.⁹

Risk factors and pathophysiology

The main risk factor for developing VAP is the presence of an endotracheal tube. The tube interferes with the normal protective mechanism of the upper airways including an effective cough. It also facilitates microaspiration of contaminated oropharyngeal secretions, which is the main pathophysiolpogic mechanism for VAP. The incidence of VAP is significantly lower with non-invasive ventilation.⁹

Commonly after intubation with an inflated cuff, colonization of the oropharynx rapidly occurs. These contaminated secretions accumulate above the inflated cuff and slowly gain access to the airway via folds in the wall of the cuff. A bacterial biofilm gradually forms on the inner surface of the endotracheal tube. This biofilm serves as a nidus for infection. With each breath, bacteria with its biofilm are propelled into the distal airways.⁹

Immunosuppression associated with critical illness is a key risk factor for the development of VAP. There is also a significant reduction of the phagocytic activity of the neutrophils with critical illness. This finding has been consistent and precedes the development of VAP.9

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