Fig. 20.1
Representative image of the CT chest upon admission
Question
What would be the best empirical therapy for this patient?
Answer
Ceftriaxone, azithromycin, and linezolid.
Because of additional concern for meliodosis, the patient was started on ceftazidime, azithromycin, and vancomycin. He developed progressive hypoxemia and agitation, at which time he was intubated and started on mechanical ventilation. Bronchoscopic bronchoalveolar lavage (BAL) of the right lower lobe revealed 240 WBCs with 81 % neutrophils. Sampling of a rapidly progressing pleural effusion showed a pleural fluid pH 6.95, glucose 44 mg/dL and LDH 1842 IU/L. Gram stain of both fluids revealed clusters of gram positive cocci. Chest tube drainage of the right pleural space was performed. Urinary antigen testing for Streptocococcus pneumoniae and fungal serologies were negative. He was empirically switched from vancomycin to linezolid. BAL and pleural fluid cultures grew methicillin-resistant Staphylococcus aureus (MRSA). Serum immunoglobulins (IGs) were subsequently found to be very low and he was given IVIG. After a prolonged ICU course, he was ultimately discharged to an acute rehabilitation facility and subsequently returned to full functional status. He continues to receive intermittent outpatient IVIG.
Principles of Management
Site-of-Care Decisions
Patients admitted to the ICU with severe community-acquired pneumonia (CAP) generally fall into one of two categories: (1) those whose symptom severity or co-morbid conditions require ICU admission at presentation and (2) those who transfer to the ICU later because of progressive decline despite receiving inpatient therapy.
Patients in need of mechanical ventilation or vasopressor support because of septic shock automatically require intensive care. However, the decision to admit to the ICU is more difficult when such obvious needs are not present. Early identification of patients likely to deteriorate is important as increased mortality is associated with ICU transfer for delayed respiratory failure or onset of septic shock. Pooled analysis of four prospective CAP studies, of which 138 had delayed-transfer compared to 315 direct Emergency Department (ED) to ICU admissions, demonstrated that the delayed-transfer group had higher 28-day mortality (23.4 % vs. 11.7 %, p < 0.02) and hospital length of stay (13 days vs. 7 days, p < 0.001) in propensity-matched analysis [1].
While some delayed transfers to the ICU represent progressive pneumonia despite appropriate treatment, many patients have subtle clinical findings upon presentation that predict a more aggressive approach will lead to improved outcomes. Using the presence of ≥3 IDSA/ATS minor criteria (Table 20.1) [2] in the ED, a before/after quality improvement project demonstrated decreased mortality (adjusted odds ratio [OR] 0.24, 95 % confidence interval [CI] 0.09–0.670, p = 0.006), fewer delayed ICU transfers (14.8 % vs. 32 %, p < 0.001), and minimal increase in direct admissions to the ICU when an aggressive pre-ICU assessment and resuscitation protocol was utilized [3].
Table 20.1
IDSA/ATS minora criteria for severe community acquired pneumonia
Respiratory rateb ≥ 30 breaths/min |
PaO2/FiO2 ratiob ≤ 250 |
Multilobar infiltrates |
Confusion/disorientation |
Uremia (BUN level, ≥20 mg/dL) |
Leukopeniac (WBC count, <4000 cells/mm3) |
Thrombocytopenia (platelet count, <100,000 cells/mm3) |
Hypothermia (core temperature, <36 °C) |
Hypotension requiring aggressive fluid resuscitation |
The Pneumonia Severity Index (PSI) and CURB-65 Score, while useful in predicting 30-day mortality and need for hospital admission, have limited ability to predict the need for intensive respiratory monitoring or vasopressor support initially. In addition to the IDSA/ATS minor criteria, several other scores such as SMART-COP [4] generally have very good sensitivity if the threshold is set optimally. However, such scoring tools will lead to a significant increase in ICU admissions if followed rigorously, and they require prospective validation.
Diagnostic Testing
Aggressive diagnostic testing is most useful in those with severe CAP requiring ICU admission and in those with risk factors for healthcare-associated pneumonia (HCAP). In such patients, the probability of finding a pathogen resistant to usual CAP empirical therapy (e.g. Staphylococcus aureus or Pseudomonas aeruginosa) is increased, and identification of a specific pathogen can lead to tailored antimicrobials, thus decreasing cost and exposure to unnecessary medications [5].
In a patient invasively ventilated, direct access to the lower respiratory tract provides the opportunity to perform an endotracheal aspirate or bronchoalveolar lavage (BAL). Moreover, bronchoscopic BAL can be useful in those where sputum or blood cultures do not yield a pathogen. In a prospective study of 262 patients admitted with CAP, fiberoptic bronchoscopic BAL provided additional diagnostic value in 49 % of patients who could not expectorate sputum and 52 % who had treatment failure 72 h after admission [6].
Blood and sputum cultures generally have low sensitivity but should still be performed upon transfer to the ICU, even in the non-intubated patient. Growth inhibition by antibiotics decreases the diagnostic yield of both tests but less so when S. aureus or gram-negative bacilli are the predominant pathogen [2]. Pleural fluid sampling is necessary in a CAP patient with a large pleural effusion (either upon admission or one which develops after empirical treatment for CAP), as a complicated pleural space requires adequate drainage.
Urinary antigen testing has reasonable sensitivity and excellent specificity for detecting Streptococcus pneumoniae and Legionella pneumophila serogroup 1. The test can stay positive for over 3 days in patients with S. pneumoniae and for weeks with L. pneumophila [2]. Although antibiotic sensitivity data cannot be obtained, the test is qualitatively important to verify that an antibiotic regimen adequately covers such pathogens.
Viral testing is important, especially in the appropriate season. A positive influenza test in a critically-ill patient should be an impetus for antiviral therapy, which can hasten disease resolution and decrease spread.
Microbial Culprits
Microorganisms responsible for CAP in the ICU mirror those of the outpatient setting, with the addition of gram-negative pathogens and MRSA. A review of 9 studies of patients with CAP admitted to the ICU showed that the most common typical bacterial pathogens were S. pneumoniae, L. pneumophila, Haemophilus influenzae, aerobic gram-negative bacilli, and S. aureus [7]. The relative frequency of atypical pathogens in the ICU setting is unclear because of heterogeneity in diagnostic technique but is approximately 20 % [2]. Respiratory viruses, either as a pure or co-infection, can be detected in up to 49 % of severe pneumonias. Common culprits include parainfluenza virus, human metapneumovirus, influenza A and B, respiratory syncytial virus, and adenovirus [8, 9]. Much less common viral pathogens include coronaviruses, such as the SARS virus and Middle East respiratory syndrome coronavirus (MERS-CoV), parechoviruses, and enteroviruses.
Epidemiologic risk factors are helpful to suggest less common etiologies (Table 20.2). Structural lung disease (e.g. COPD with repeated exacerbations or bronchiectasis), prior hospitalization and healthcare exposure pose an increased risk of Pseudomonas, chronic alcoholism is a risk for other gram-negative pathogens (Klebsiella pneumoniae or Acinetobacter species), and end-stage renal disease, injection drug use, prior influenza infection, and prior treatment with fluoroquinolones pose an increased risk of S. aureus [2].
Table 20.2
Epidemiologic conditions and/or risk factors related to specific pathogens in community-acquired pneumonia
Condition | Commonly encountered pathogen(s) |
|---|---|
Alcoholism | Streptococcus pneumoniae, oral anaerobes, Klebsiella pneumoniae, Acinetobacter species, Mycobacterium tuberculosis |
COPD and/or smoking | Haemophilus influenzae, Pseudomonas aeruginosa, Legionella species, S. pneumoniae, Moraxella catarrhalis, Chlamydophila pneumoniae |
Aspiration | Gram-negative enteric pathogens, oral anaerobes |
Lung abscess | CA-MRSA, oral anaerobes, endemic fungal pneumonia, M. tuberculosis, atypical mycobacteria |
Exposure to bat or bird droppings | Histoplasma capsulatum |
Exposure to birds | Chlamydophila psittaci (if poultry: avian influenza) |
Exposure to rabbits | Francisella tularensis |
Exposure to farm animals or parturient cats | Coxiella burnetti (Q fever) |
HIV infection (CD4 > 200) | S. pneumoniae, H. influenzae, M. tuberculosis |
HIV infection (CD4 < 200) | The pathogens listed for early infection plus Pneumocystis jirovecii, Cryptococcus, Histoplasma, Aspergillus, atypical mycobacteria (especially Mycobacterium kansasii), P. aeruginosa, H. influenzae
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