Pneumonia is an infection of the lower respiratory tract in which the respiratory zone has become infected. The causative agents could be bacterial, viral, or fungal. 

Pneumonia classifications are based on the clinical setting in which the patient has become ill. The exact causative agents of any pneumonia varies with the patient’s age, and general health. Patients who live in nursing homes will get different infections from healthy people who get sick at home. People who live in dormitories, prisons and military camps will catch different infections from the rest of us. Patient who are immune-suppressed from radiation, chemotherapy or disease will catch infections from opportunistic micro-organisms as well as the microbes that prey on the rest of us.  

Pathophysiology of Pneumonia 

·         Because pneumonia affects the alveoli, there will be exudates & cellular debris in the alveoli and interstitial spaces. This consolidation of the alveoli will decrease lung compliance because the alveoli are stiff and harder to inflate. This leads to increased WOB

·         There will be hypoxemia because the PA0₂ is decreased due to:

o    decreased surface area for gas exchange as alveoli fill with secretions

o    decreased diffusion because the actual alveolar wall can be thickened due to inflammation

o    If relatively localized, there may be a V/Q mismatch that can be corrected by supplementary 0₂

o    If extensive enough there can be a physiological shunt because the alveoli filled with secretions are perfused without ventilation. 0₂ will not help at this point.

·         Interstitial edema: another cause of hypoxemia is due to the swelling of the interstitial spaces with fluid and inflammatory substances so that there is less diffusion into the capillaries and the lungs become even stiffer

·         If the causative agent is a necrotic bacteria, such as Klebsiella or Tuberculosis, there can be areas of necrosis, cavitations or abscess with resulting hemoptysis and even pneumothorax

·         Fluid can ‘weep’ into the chest cavity and cause effusions that further decrease the lung compliance and can cause atelectasis of the adjacent lung segments.

·         Fluid can ‘weep’ into the fissures causing effusions that can press on adjacent lung segments causing atelectasis. 

Classification by Population at Risk 

Community-acquired infections are further classified as typical and atypical and chronic and acute.  A typical pneumonia would be something like pneumococcal, Streptococcus Pneumoniae & H. Influenzae, while atypical pneumonias would be due to more rare microbes such as Legionella & Mycoplasma. In addition to happening less often, the atypical also present with different sets of symptoms from typical pneumonias as seen in s/s section of these notes. 

Nosocomial pneumonias are diagnosed when the patient gets symptoms 48 hours or more after being admitted. Because the hospital patient is frequently immuno-compromised in an environment filled with pathogens, the causative agents of Nosocomial pneumonia is less likely to be the typical community-acquired pneumonia. Pseudomonas A. is an example of a nosocomial pneumonia.  

Nosocomial pneumonias are further classified by those suffered by intubated patients [VAP] and non-intubated patients and then there is an entire list of rare bacterial infections found in the nursing home patient. These are frequently antibiotic-resistant bacterial infections. 

Nursing Home Acquired Pneumonia 

Aspiration pneumonias are found in patients who cannot protect their airways such as persons who abuse ethanol and other sedatives. Patients who have suffered strokes or other neurological disorders are also at increased risk for aspiration pneumonias. Aspiration pneumonias tend to be seen as lobar bacterial pneumonias & are frequently caused by gram + and anaerobic bacteria. Intubated patients are at increased risk of aspiration pneumonias particularly if the cuff is not inflated properly. 

The actual site for the lobar pneumonia depends on the patient’s position when he aspirated. “Favored segments for aspiration in the recumbent position are the superior segment of a lower lobe or the posterior segment of an upper lobe, and those in the upright position are the lower lobes.”  

“The oral cavity is densely populated by site-specific flora. Patients with advanced periodontal disease are at particular risk for the development of aspiration pneumonitis”

Go here for x-rays and more descriptions of aspiration pneumonia: Aspiration Diseases: Findings, Pitfalls, and Differential Diagnosis  

Classification of Pneumonia by Foci 

Some infections start in a segment or lobe and stay there or move to adjacent segments or lobes. Bacterial infections tend to start in segments or lobes. The pneumonia will be classified as “lobar pneumonia.” 

Other infections are spread through the blood-stream & can result in a diffuse infection. These blood-borne infections are usually viral such as the flu and adenovirus.  

Rarely an infection starts in a distant organ such as an infected heart valve and the bacteria moves to the lung via the blood-stream. Other rare infections can start in an adjacent organ such as the liver and spread through the diaphragm into the lung. 

Classification of Pneumonia by its Ability to Become Dormant or Latent. 

Tuberculosis is an example of a bacterial infection that can be latent and re-occur years after initial inoculation. This usually happens after a patient becomes immuno-suppressed or seriously physically stressed.  

Other examples are Pneumocystis carinii [PCP] & Cytomegalovirus [CMV] pneumonia. Both organisms are present in most of us and appear as a disease only in persons with full-blown AIDS or other severe immuno-compromised conditions. 

S/S of pneumonia 

Typical presentation: sudden onset of high fever, chills & pleuritic chest pain, followed by cough. If productive, it may be rusty-colored because it is coming from alveoli and the secretions are stained by RBC's.  

Due to the increased WOB seen with decreased lung compliance, there will be rapid, shallow breathing. Increased WOB and fever can cause tachycardia. Due to increased WOB, there will be increased use of accessory muscles, poor chest excursion & nasal flaring.  

Due to hypoxemia, there can be tachypnea, tachycardia and cyanosis. Based on the degree of illness the patient may or may not have hypoxemia, but only when the patient gets seriously ill will there be hypercapnia. When the patient has uncompensated respiratory acidosis with moderate to severe hypoxemia, he is going into respiratory failure and needs to be intubated and ventilated. 

atypical presentation: headache, gradual increase in fever, diarrhea and unproductive cough or scanty secretions. Some atypical pathogens can cause a bradycardia. If there is a chronic infection such as some of the fungal infections, there could be weight loss and night sweats.  

The cold agglutinins test is performed to detect the presence of antibodies in blood that are sensitive to temperature changes this includes Mycoplasma pneumonia [walking pneumonia]

Cold agglutinins test 

S/S in the elderly: the elderly are frequently dehydrated so that the BBS and the cough is not noticeable. They may not present with a fever, but have confusion or worsening of CHF. 

Bilateral BBS

Classically, in the person without underlying COPD or asthma, there will be crackles over the affected area due to the atelectasis, but if the patient has a viral infection such as the flu, he may present with diffuse wheezing in addition to the crackles.  

If there is bronchopneumonia, there will be rhonchi and crackles.  

If there is significant atelectasis, there could be diminished breath sounds in the affected area.  

Because 1/3 of patients with bacterial pneumonia get pleura effusions, you might hear a plural rub over the affected area.

Percussion

There will be dullness to percussion over areas of consolidation, effusions and atelectasis. If there is pleurisy or effusion, the patient could demonstrate tenderness to palpation 

Lab

WBC will be increased in infection as leukocytes increase to fight the infection. If viral infection is present, one sees increases in lymphocytes.  

If bacterial, one sees increases in neutrophils.  

If there are increased segmented neutrophils, the infection has lasted long enough for the body to throw immature neutrophils at the bacteria.  

Naturally, if the patient is immune-suppressed, we may have no increases.  

Sputum 

If bacterial infection is suspected, we get sputum for C & S and for gram stains.  

If TB is suspected after a + PPD, and with X-ray proof of active pulmonary disease, we will get a sputum for AFB [acid-fast bacilli] 

Anaerobic bacteria will have quite smelly sputum & if the pus comes from an abscess that ruptured there could be a sudden influx of massive amount of smelly sputum for a short time. 

Some diseases are difficult to diagnosis because they require bronchial washings, biopsies or brushings obtained during bronchoscope. Legionella & PCP are two that require a deep sample. 

Blood work & other fluids 

If viral infections are suspected, we can get an ELISA or blood titers of antigens for proof of exposure.  

Go here for a discussion of the ELISA test for HIV ELISA 

Because a 3rd of bacterial pneumonias present with some organism in the bloodstream, a blood culture for gram stain and C & S may also be helpful. 

If there is large enough effusion, it can be aspirated by needle and cultured to make sure the effusion is not a secondary infection. Effusions are frequently anaerobic bacteria so the fluid might be smelly.

Skin tests  

If fungal infections are suspected, the patient gets skin testing for specific fungi or a serological test of complement fixation.

Serological Tests

ABG

Because of the alveolar hypoxia, hypoxemic hypoxia can result in varying degrees of hypoxemia from mild to moderate to severe to refractory. 

Under normal conditions, a healthy person with pneumonia will have normal C0₂ levels, but if the patient goes into respiratory failure, there can be a rise in the PaC0₂ and uncompensated respiratory acidosis.

PFT 

We don’t generally do PFT's for patients with pneumonia, but we would expect the FRC in severe cases to be down as the RV drops in the face of alveolar collapse. This is a restrictive defect with low compliance. 

Diffusion of 0₂ will be decreased because alveolar ventilation is decreased, surface area for diffusion is decreased and the thickness of the alveolar-capillary membrane may be increased by thickened type I cell & by interstitial swelling from influx of fluid and WBC. 

If there is wheezing such as with viral pneumonias, the expiratory flow rates will be decreased, which may or may not respond to bronchodilators.

Chest films 

Most pneumonia has areas of alveolar consolidation, in which we see white [radio-opaque] alveolar opacities with dark air bronchograms running across them. These consolidations could be diffuse, segmental or even lobar. 

If there is interstitial pneumonia we may see reticular densities [linear] but it is not uncommon to see both consolidation and reticular patterns in the same person. 

If the consolidation has resulted in atelectasis, we see intercostal spaces over the atelectasis that are closer together, or a hemidiaphragm or fissure that has moved into the vacuum left by the collapse. 

Early pneumonias may have no X-ray changes at all.  

There are some x-ray s/s specific to certain types of pneumonia  

Bacterial pneumonias tend to cause the following X-ray signs

·         pleura effusions

·         lobar or segmental infiltrates

·         abscesses

·         cavitations

·         Areas of necrosis which could lead to hemoptysis or even pneumothorax.  

Bronchopneumonia can have patchy infiltrates and the patient will have rhonchi and the cough is effective.  

Tuberculosis: has an affinity for the well-ventilated upper lobes. It may present with cavitations that damage the lung that can eat into blood vessels. Older TB lesions leave scars. Hilar and mediastinal lymphatic swelling may be seen & in some kids, TB can cause RML syndrome.  

If the infection becomes disseminating TB, spread by the bloodstream, there will be a diffuse miliary pattern in the lung. These are tiny white round densities like a millet seed. 

Fungal pneumonia can present with cavitations, and aspergillosis can display a fungal ball.  

Viral pneumonias tend to have the following x-ray s/s

·         interstitial linear patterns 

·         will be diffuse rather than in a single lobe

·         can more easily progress to ARDS.

PCP pneumonia shows up like a viral infection with a diffuse interstitial pattern.  

Legionella [a bacteria] pneumonia will start in a single lobe and within 24-48 hours move quickly to the rest of the lung. These infections are caused by exposure to aerosols in air-conditioning.  

Staph A [a bacteria] can develop a pneumatocele, which is a bulla that forms in about 24 hours.

Varicella [chicken pox] pneumonia will present with diffuse miliary pattern. 

Complications of pneumonias: 

·         worsening of infection to include sepsis and septic shock which can lead to death

·         can trigger ARDS which has a high mortality

·         supra-infection  from improper antibiotic use

·         bronchiectasis can complicate many serious pulmonary infections causing permanent damage

Pneumonia and respiratory failure: most patients with pneumonia don’t need to be intubated and ventilated-- but we need to move fast with the ones who do.

·         The patient with pneumonia can present with hypoxic respiratory failure due to refractory hypoxemia. If the Fi02 is above 50 % with a Pa02  less than 50 torr, we need more than supplementary 02. We need to increase the volume inside the alveoli by application of PEEP or CPAP

·         He can present with hypercapnic respiratory failure due to fatigue from increased WOB, if his required driving pressure is increased enough by decreased compliance and/or increased RAW. If the Pac0₂ rises above 55 torr and the pH drops below 7.20, he needs to be intubated & ventilated.

o    As the patient’s Vt drops from poor compliance and his respiratory rate rises to compensate, he just moves more Vd ventilation faster. This is unproductive [Vd/Vt more than .6]

o    Or if the patient’s spontaneous Ve rises above 10 lpm to maintain his ABG, he will eventually suffer fatigue.

Treatment

·         proper use of the correct anti-microbial agent is critical

·         good systemic hydration to mobilize secretions

·         antipyretics and analgesics for fever and pain

·         If patient is in respiratory distress, avoid giving sedation & cough suppressants. Once he is intubated and ventilated, sedation and even paralytic agents are safe.

·         good pulmonary hygiene: if excessive secretions warrant it, mucolytics and CPT/PD or other adjuncts, but remember that CPT is contraindicated in cases complicated by effusions

·         if he cannot cough effectively because he cannot move 10 ml/kg IBW, consider starting IPPB starting at 12-15 ml/Kg Vt to reverse atelectasis and deliver medications

·         Based on the patient’s baseline 0₂ status, monitor Sp0₂ or ABG & treat hypoxemia. Watch for refractory hypoxemia because diffuse alveolar problems are problematic & prone to this.

·         if present, treat bronchospasm with short-acting Beta II agonists.

·         if the patient presents with uncompensated respiratory acidosis [7.25 or less] with moderate-severe hypoxemia, consider intubation and ventilation.

o    If the RAW and compliance are basically normal, we can  start with  VC or SIMV mode.

o    If the RAW and compliance are basically normal, we can give a rate of 10-12 bpm and a Vt of 10-12 ml/kg IBW

o    Flow rate of 60-80 lpm to get the I:E ratio to 1:2 or 1:3 –unless there is bronchospasm and prolonged exhalation is needed. In this cause increased the flow rate and decrease the respiratory rate [f] to allow time to exhale.

o    Any persons who are sick enough to get intubated & ventilated for pneumonia are at risk for ARDS--- so we may need to change the mechanical ventilation protocol if it is impossible to ventilate and oxygenate the patient without raising the P Plateau above 30 cmH20 

o    If the hypoxemia is refractory, give PEEP* and start to wean the Fi02 below the toxic levels.

o    We may need to ventilate a patient for 24-48 hours to rest them  

o    If the pneumonia is unilateral or lobar, be aware that the PEEP may only over-inflate the good part of the lung and decrease its capillary blood flow causing a high V/Q mismatch.

·         If excessive secretions are present, hyper-inflate, irrigate and suction to keep ET tube clear

·         If secretions change or a new infiltrate appears on the X-ray, consider a supra- infection. Get new sputum culture and sensitivity and be ready to change or even add new antibiotics.

·         If localized atelectasis persists in spite of good pulmonary hygiene, a therapeutic bronchoscope might be needed to remove the impacted secretions.