Pneumonia & pulmonary parenchyma

Pneumonia is a pulmonary parenchyma infection and a leading cause of fatality and morbidity. Despite of its perilous threats, pneumonia is commonly underestimated, misdiagnosed, and mistreated. Earlier, this disease was believed to be acquired not only from the community and from the hospital but also through ventilator-associated cases (Chastre and Fagon, 2002). But for about two decades, most diagnosed pneumonia was cases of multidrug-resistant or MDR pathogens acquired through hospital-related causes.

The hospital-acquired cases of pneumonia were attributed to the potent oral antibiotic utilization, early transfer of acute-care patients from the hospital into their homes, low-acuity facilities, prevalence of the outpatient IV antibiotic therapy applications, extensive immunomodulatory therapies and aging (Vanderkooi, Low, Green, Powis, and McGeer, 2005). The detection of the MDR pathogen involvement has resulted to the re-classification of infection as Healthcare-Associated Pneumonia or HCAP and Community-Acquired Pneumonia or CAP.

The former classification has subcategories which include ventilator-associated pneumonia or VAP and hospital-acquired pneumonia or HAP. Even though the new classification system has paved for an effective design of antibiotic treatment, disadvantages are still at hand (Stone and Humphries, 2008). However, some MDR pathogens are not considered as risk factors; thus, the screening of factors for individual cases should be done.

For instance, the risk factors for MDR infection of a dementia patient with capability of feeding and dressing herself is entirely different from a patient in the chronic vegetative state under tracheostomy with percutaneous feeding tube condition. Additionally, the risk factors for MDR infection do not exclude CAP development (Stone and Humphries, 2008). Pathophysiology Pneumonia resulted from the host’s response to the alveolar infection caused by microbial pathogens (McPhee and Ganong, 2006). Typically, these pathological microorganisms penetrate the lower respiratory tract through oropharynx.

During sleep or low-level of consciousness, small-volume inhalation of pathogen-contaminated droplets may occur in the individual. Pneumonia infrequently undergoes a hematogenously spread such as from tricuspid endocarditis or by the adjacent extension from the infected mediastinal or pleural space (McPhee and Ganong, 2006). As defense, the host largely depends on the turbinates and hairs of the snares which seize inhaled particles upon penetrating the lower respiratory tract as well with the branching structures of the tracheobronchial tree which catch inhaled particles away from the lining of the airway (McPhee and Ganong, 2006).

In such way, other local antibacterial factors or mucociliary clearance kill or paralyze the inhaled microorganisms. In connection to this, cough mechanism and gag reflex provide protection from inhalation. Moreover, the natural flora in the oropharynx’s mucosal cells hinders the adherence of the pathogenic bacteria which eventually lessens the risk of pneumonia development (McPhee and Ganong, 2006). Further, when the microorganisms still hurdle the aforementioned barriers, alveolar macrophages attack the pathogens.

Through local proteins with antiviral or antibacterial properties, the macrophages kill or paralyze the penetrating pathogens (McPhee and Ganong, 2006). After swallowing up the microorganisms, the macrophages are transported out by means of the lymphatics or mucociliary elevator (McPhee and Ganong, 2006). However, when their capabilities for engulfing were superceded by microorganisms, the infection will clinically manifest.

As a consequence, the alveolar macrophages induce inflammatory response to boost the mechanism of defense in the lower respiratory tract. Thus, the inflammatory response of the infected individual generates the clinical symptoms of the disease. In particular, the production of tumor necrosis factor or TNF and interleukin or IL 1 causes fever (Hanley and Welsh, 2003). As well, the actions of granulocyte colony-stimulating factor and Chemokines like IL-8 produce neutrophils which trigger purulent secretions and leukocytosis in lungs (McPhee and Ganong, 2006).

Nevertheless, the neutrophils along with the inflammatory substances generated by macrophages stimulate alveolar capillary leak similar to ARDS or acute respiratory distress syndrome. Meanwhile, erythrocytes also penetrate the alveolar-capillary membrane causing hemoptysis. This leak leads to radiographic infiltrate and detection of rales on auscultation while alveolar filling results to hypoxemia. On the other hand, some pathogens obstruct the hypoxic vasoconstriction, normally seen in fluid-filled alveoli, that triggers hypoxemia severity (Hall, Schmidt, and Lawrence, 2005).

The elevated respiratory drive in the SIRS or system inflammatory syndrome results to respiratory alkalosis while dyspnea is a result of compliance lowering created by the elevated respiratory drive, infection-related bronchospasm, hypoxemia, increased secretions, and capillary leak (Hall, Schmidt, and Lawrence, 2005). At worse, the severity of these symptoms induces lung volume decreased and compliance reduction as well as lung mechanic changes and intrapulmonary blood shunting which eventually trigger the death of the infected individual. Pathology

The initial phase of the pathological changes in classic pneumonia is edema in the presence of bacteria and proteinaceous exudates in alveoli (Estrada, Unterborn, Price, Thompson, and Gibson, 2000). This phase is swiftly fallowed by the red hepatization phase, the second phase, as characterized by the presence of neutrophils and erythrocytes in the intraalveolar exudates (Estrada, Unterborn, Price, Thompson, and Gibson, 2000). Then, the gray hepatization is the third phase wherein the erythrocytes from the second phase undergo lysis and degradation as new erythrocytes extravasate (Estrada, Unterborn, Price, Thompson, and Gibson, 2000).

Also, bacteria in this phase seem annihilated as fibrin and neutrophil are predominantly observed. Thus, the third phase is an indication of satisfactory pathogen containment leading to an improved gas exchange. Lastly, in the resolution phase, the bacteria, neutrophils, and fibrin debris created by inflammatory response have been eliminated and the macrophages are mainly observed (Estrada, Unterborn, Price, Thompson, and Gibson, 2000). However, these phases are only applicable to pneumonia cases caused by pneumonococcal bacteria.

For VAP, prior to the generation of radiologically apparent infiltrate, the respiratory bronchiolitis is observed (Mayhall, 2001). As brought by the microaspiration mechanism, the bronchopneumonia pattern is typical in the cases of nosocomial pneumonias while the lobar pattern is common in the cases of bacterial CAP (Hanley and Welsh, 2003). Nonetheless, pneumocystis and viral pneumonias involve alveolar process rather than interstitial regardless of radiographic observation. Etiology

The list of CAP pathogen includes protozoa, viruses, bacteria, and fungi as well as the recently identified metapneumoviruses, the MRSA or the community-acquired and methicillin-resistant strain of Staphylococcus aureus, hantaviruses, and the coronavirus of SARS or the severe acute respiratory syndrome. Even though the Streptococcus pneumoniae is the most common pathogen, other microorganisms may aggravate the clinical conditions of the patient (Lewis and Macfarlane, 2003). As such, other potential pathogens may include typical bacteria like Klebsiella pneumoniae, S.

aureus, Pseudomonas aeruginosa, and Haemophilus influenzae while atypical bacteria include Legionella spp. , Chlamydophila pneumoniae, and Mycoplasma pneumoniae along with RSVs or respiratory syncytial viruses, adenoviruses, and influenza viruses (Lutfiyya, Henley, and Chang, 2006). Based on medical records, 18% of CAP cases were caused by viruses wherein about 10-15% of these cases were ascribed to infections brought by the atypical and typical bacterial pathogen combination or polymicrobial (Lewis and Macfarlane, 2003).

As the atypical bacteria are unable to be cultured nor observed on the Gram’s stain, the pathogens like Legionella in inpatients as well as the C. pneumoniae and M. pneumoniae in outpatients are of prime importance for the determination of drug treatment. These microorganisms are highly resistant to ? -lactam and can only be treated with tetracycline, fluoroquinolone, and macrolide (Singh, Rogers, Atwood, Wagener, and Yu, 2000). On the other hand, the disease can be attributed to anaerobes when the aspiration case was observed for several days or weeks upon the symptoms of pneumonia.

The cases of anaerobic pneumonia are accompanied by empyemas or parapneumonic effusions and abscess formation (Hanley and Welsh, 2003). In addition, unprotected airway such as in patients with seizure disorder and gingivitis as well as substance abuse patients aggravate the risk factors. In line with these, the influenza infection is complicated by S. aureus pneumonia while CAP was recently ascribed with MRSA strains. Medical practitioners must be conscious on the implication of such cases like the development of necrotizing pneumonia.

These scenarios were postulated on the proliferation of MRSA strains from the hospital into the community and on the appearance of new MRSA strains in the community (Lutfiyya, Henley, and Chang, 2006). Consequently, the new community-acquired MRSA or CA-MRSA strains infected individuals who were not formerly associated with healthcare. Unluckily, in CAP cases, no matter how intensive radiographic and physical examinations be conducted, the pathogen can hardly be identified. Clinical manifestation The CAP patients manifest indolent to fulminant symptoms with mild severity to fatal case (Lutfiyya, Henley, and Chang, 2006).

The variation of the clinical symptoms is largely influenced by the severity and progression of the infection but limited to the complications on lung and its related structures. As such, the infected individual is most often febrile and experiences sweating, chilling with tachycardic response, as well as productive or nonproductive cough with respect to blood-tinged sputum, purulent or mucoid (Lutfiyya, Henley, and Chang, 2006). Along with these, the patient may also experience breathing difficulties depending on the severity of the disease and pleuritic chest pain on the presence of pleura.

As well, about 20% of pneumonia cases, diarrhea, arthralgias, nausea, headache, myalgias, fatigue, and vomiting are observed (Lutfiyya, Henley, and Chang, 2006). Meanwhile, physical assessment involves variations on pleural effusion and pulmonary consolidation. Specifically, the use of accessory muscles in respiration and increased rate of respiration are the most common symptoms. In addition, changes in the tactile fremitus can be detected through palpation whereas the dull and flat percussion note respectively signifies the consolidated and pleural fluid (Brown and Gilford Jr. , 2004).

Nonetheless, a pleural friction rub, crackles, and bronchial breath sounds are heard during auscultation (Brown and Gilford Jr. , 2004). These clinical symptoms are hardly examined in elderly patients under the worsening or new-onset stage of the disease but those in severe conditions with septic shock imparted by CAP are hypotensive and may experience organ failure. Clinical Management In dealing with CAP or HAP medication, there are general considerations that should be taken into account. Particularly, for hypoxemia patients, adequate hydration and ventilation are necessary for an effective treatment.

Despite the fluid resuscitation and the positive response to glucocorticoid treatment, individuals with severe CAP cases are hypotensive and suffer from adrenal insufficiency (Fine et al. , 1997). Further, for those with septic shock and S. pneumoniae infection, immunomodulatory therapy by means of activated drotrecogin alfa is advised to be employed. Still, failure to respond to therapy necessitates the reassessment of the clinical conditions at approximately three days of non-improving conditions (Hanley and Welsh, 2003).

This failure to elicit a positive response can be attributed to either the pathogen resistance to the drug or to the disease complications such as empeyema of lung abscess which block the actions of the antibiotic against the microorganisms. Likewise, non-improvement of the patients’ conditions may entail that they are receiving either wrong drug treatment or drug treatment in the wrong frequency or administration dose. In connection to these, it is possible that in the CAP diagnosis, the specific pathogen was falsely identified. Additionally, the nosocomial superinfections are also possible causes of the disease persistence.

On the other hand, several non-infection conditions like connective tissue troubles in lungs, lung carcinoma, pulmonary edema, radiation and hypersensitivity pneumonitis, and pulmonary embolism may project symptoms similar with pneumonia clinical manifestations (Hanley and Welsh, 2003). Hence, reevaluation of the patients’ conditions after delayed response through bronchoscopy and computed tomography should be conducted to prevent deteriorating conditions. Home-based treatment may suffice for some cases of pneumonia while other patients need intensive treatment in the hospital.

Thus, assessment instruments are crucial for the formulation of a sound decision concerning the medication treatment of the patients. Presently, the CURB-65 criteria and the Pneumonia Severity Index, PSI, are commonly utilized for the evaluation of unnecessary hospital admission, severity of the disease, adverse treatment outcomes, and even possible death (Brown and Gilford Jr. , 2004). In PSI, twenty variables are incorporated which include, physical examination and laboratory tests findings, coexisting disease of the patient and his or her age.

Then, the patient will be classified based on the resulting score with its respective rate of fatality: class 1, 0. 1%; class 2, 0. 6%; class 3, 2. 8%; class 4, 8. 2%; and class 5, 29. 2% (Stone and Humphries, 2008). Based on clinical studies, the utilization of PSI instrument often led to the hospitalization of class 4 and class 5 patients while the 1 and 2 classes are sparingly admitted in the hospital. Also, the class 3 patients are encouraged to be admitted in the hospital for an intensive observation until such time that a sound decision will be made.

On the other hand, the CURB-65 criteria include age, respiratory rate, confusion, blood pressure, and urea level. Patients who have zero score in the instrument are associated with 1. 5% 30-day fatality rate while a score of 2 indicate hospital admission and associated with 9. 2% fatality rate (Myint, Kamath, Vowler, and Harrison, 2007). Nevertheless, scores of greater than 3 with associated 22% rate of mortality require patients for hospitalization under intensive care unit (Myint, Kamath, Vowler, and Harrison, 2007).

The PSI instrument seems impractical for emergency cases due to a great number of variables while the CURB-65 criteria instrument has not yet extensively proven. Whichever instrument is utilized, the variables for each with respect to the unique case of the patient must be cautiously taken into account along with the capability of the patient for oral antibiotic regimen and his or her available resources. As the clinical stable patients discharge from the hospital, their residential sites must be regarded as areas of potential risk for elderly patients. Meanwhile, vaccination is the main preventive measure for all pneumonia types.

For vaccination, the guidelines of the Advisory on Immunization Practices should strictly be imposed specifically on pneumococcal and influenza vaccines. As well, since endotracheal tube is the most risk factor for VAP, the most effective preventive measure is the endotracheal intubation (Mayhall, 2001). This can be done by means of noninvasive ventilation through nasal or full-face mask along with the strategies in the reduction of the ventilation duration (Fagon et al. , 2000). Conclusion Pneumonia is a lung infection which often times underestimated, misdiagnosed, and mistreated.

It is a result of the patient’s response to the alveolar infection caused by either microbial or viral pathogens. These disease-causing microorganisms can be acquired through hospital, community, and ventilator-related cases. As well, the MDR pathogens were found to cause pulmonary parenchyma infection. These microorganisms are highly resistant to ? -lactam and can only be treated with tetracycline, fluoroquinolone, and macrolide. The infected individual is most often febrile and experiences sweating, chilling with tachycardic response, as well as productive or nonproductive cough with respect to blood-tinged sputum, purulent or mucoid.

Consequently, the use of accessory muscles in respiration and increased rate of respiration can be observed. For hospitalization, the PSI and the CURB-65 criteria are frequently used as the decision basis. As the clinical stable patients discharge from the hospital, their residential sites must be regarded as areas of potential risk for elderly patients. For all types of pneumonia, vaccination is the most recommended preventive measure. References Brown, K. and Gilford, Jr. W. (2004). Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 6th ed.

New York: McGraw-Hill. Chastre, J. and Fagon, J. Y. (2002). Ventilator-Associated Pneumonia. American Journal of Respiratory and Critical Care Medicine, 165, 867. Estrada, C. A. , Unterborn, J. N. , Price, J. , Thompson, D. , and Gibson, L. (2000). Judging the Effectiveness of Clinical Pathways for Pneumonia: The Role of Risk Adjustment. Effective Clinical Practice, 3 (5), 221-228. Fagon, J. Y. , Chastre, J. , Wolff, M. , Gervais, C. , Parer-Aubas, S. , Stephan, F. , Similowski, T. , Mercat, A. , Diehl, J. L. , Sollet, J. P. , and Tenaillon, A. (2000).

Invasive and Noninvasive Strategies for Management of Suspected Ventilator-Associated Pneumonia. Annals of Internal Medicine, 132, 621. Fine, M. J. , Auble, T. E. , Yealy, D. M. , Hanusa, B. H. , Weissfeld, L. A. , Singer, D. E. , Coley, C. M. , Marrie, T. J. , and Kapoor, W. N. (1997). A Prediction Rule to Identify Low-Risk Patients With Community-Acquired Pneumonia. New England Journal of Medicine, 336, 243. Hall, J. B. , Schmidt, G. A. , and Lawrence, D. H. (2005). Wood Principles of Critical Care, 3rd ed. New York: McGraw-Hill. Hanley, M. E. and Welsh, C. H. (2003).

Current Diagnosis and Treatment in Pulmonary Medicine. New York: McGraw-Hill. Lim, W. S. , van der Eerden, M. M. , Laing, R. , Boersma, W. G. , Karalus, N. , Town, G. I. , Lewis, S. A. , and Macfarlane, J. T. (2003). Defining Community-Acquired Pneumonia Severity on Presentation to Hospital: An Internatiuonal Derivation and Validation Study. Thorax, 58, 377. Lutfiyya, N. M. , Henley, E. , and Chang, L. F. (2006). Diagnosis and Treatment of Community-Acquired Pneumonia. American Family Physician, 73 (3), 442-450. Mayhall, G. C. (2001). Ventilator-Associated Pneumonia or Not?

Contemporary Diagnosis. Emerging Infectious Disease, 7 (2), 200-204. McPhee, S. J. and Ganong, W. F. (2006). Pathophysiology of Disease: An Introduction to Clinical Medicine, 5th ed. New York: McGraw-Hill. Myint, P. K. , Kamath, A. V. , Vowler, S. L. , and Harrison, B. D. (2007). Simple Modification of CURB-65 Better Identifies Patients Including the Erderly with Severe CAP. Thorax, 62, 1015-1016. Singh, N. , Rogers, P. , Atwood, C. W. , Wagener, M. M. , and Yu, V. L. (2000). Short-Course Empiric Antibiotic Therapy for Patients With Pulmonary Infiltrates in the Intensive

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