Hospital Acquired Pneumonia
Original Editors - Students from Glasgow Caledonian University's Cardiorespiratory Therapeutics Project.
Top Contributors - Bertie Elles, Lucinda hampton, Kim Jackson, Adam Vallely Farrell, 127.0.0.1, Admin, Michelle Lee, Karen Wilson and Lauren Lopez
Introduction[edit | edit source]
Hospital-acquired pneumonia (HAP) is defined as pneumonia that occurs 48 hours or more after hospital admission and is not incubating at hospital admission.
- Early-onset (occurring within 4 days of admission) HAP is usually caused by the same bacteria and viruses as community-acquired pneumonia and has a good prognosis.
- Late-onset (starting 5 days or more after admission) HAP has a worse prognosis and is usually caused by micro-organisms that are acquired from the hospital environment. MRSA, Pseudomonas aeruginosa and other non-pseudomonal Gram-negative bacteria are the most common causes."[1]
HAP is the second most common hospital acquired infection (see Healthcare-Associated Infections), catheter-associated urinary tract infections being the most common.[2]
Epidemiology[edit | edit source]
- HAP is a common cause of pneumonia in those admitted to intensive care units (ICU) or on mechanical ventilation. 9/10 cases of HAP develope in ICUs occur in patients who are intubated and mechanically ventilated.
- The elderly are more are risk of developing HAP.[3]
Investigations[edit | edit source]
HAP or VAP should be suspected in all patients, whether ventilated or not, if two or more of the following clinical features are present: temperature greater than 38°C or less than 36°C; leukopenia or leukocytosis; purulent tracheal secretions and decreased partial pressure of oxygen in arterial blood (PaO2).[4]
General investigations are not necessary for the majority of patients who are managed in the community. Pulse oximeters allow for simple assessment of oxygenation. When a patient is admitted to hospital:
FBC with differential white cell count:
Total white blood cells: All the white cell types are given as a percentage, and as an absolute number per liter. A high WBC is often an indicator of infection[5].
CRP (to aid diagnosis and as a baseline measure). The C-reactive protein (CRP) test is a diagnostic tool that identifies regions of inflammation[6]. CRP is a protein manufactured in the liver before dispersal into the blood which occurs a few hours after any form of tissue injury, an acute manifestation of infection, or inflammation caused by another source[6]. The CRP test can be used in adjunction with signs, symptoms and other tests in order to fully evaluate patients with HAP[6].
Blood cultures:
Blood culture is a microbiological culture of blood. It is employed to detect infections that are spreading through the bloodstream (such as bacteremia, septicemia amongst others).
Pneumococcal and legionella urinary antigen tests:
Urine tests are administered and designed to locate the presence of both Streptococcus pneumoniae and Legionella species[7]. Two major pathogens in HAP, which also play a key role in community acquired Pneumonia. The tests are usually in conjunction with both sputum examination and blood testing due to their high specificity[7].
CXR:
HAP may deliver signs of abnormal opacity in specific areas of the lungs, or even clear consolidation due to inflammation causing abnormal positioning of structures, such as the trachea and mediastinum[8].
Sputum examination and culture.
Sputum Examination is a diagnostic tool used to identify bacteria and fungi located in the pulmonary facet[9]. Samples are often obtained through expectorating or in some cases an induced saline can produce the required volumes from lab testing. HAP normally produces sputum in a thick and purulent form, which is common in more cases of infection[9].
Blood gases:
Blood gases will demonstrate how well both the respiratory and the renal systems are functioning[10]. In terms of HAP ABG’s can be used to gain insight into the patient’s oxygen saturation levels as well as demonstrate incidences of both acidosis and alkalosis, both of which can occur due to poor ventilation[10].
Aspiration of pleural fluid (for biochemistry and culture).
Chest aspiration is a diagnostic tool used to investigate the cause of pleural fluid or to improve respiration rates that have dropped due to accumulated fluid[11]. Samples of the pleural fluid are sent for analysis which includes cytology for malignant cells and bacteriology for identification of foreign bacteria[11].
Clinical Manifestations[edit | edit source]
Symptoms of HAP: includes cough, expectoration, a rise in body temperature, chest pain or dyspnea.
Signs include of HAP include: fever, tachypnea, consolidations or crackles.[12]
The time of onset of HAP is a large determinate of the type of bacteria causing the infection:
- Early-onset HAP occurring in the first 4 days of hospitalization) is often caused by community-acquired pathogens such as:
Haemophilus influenzae,
Streptococcus pneumoniae, or
methicillin-susceptible S aureus (MSSA).
In this context, pathogens with strong intrinsic or acquired antimicrobial resistances are rarely causative. - Late-onset HAP developing ≥ 5 days after hospitalization is often caused by aerobic Gram-negative bacilli such as:
P aeruginosa,
Enterobacteriaceae, or
Acinetobacter) or
Methicillin-resistant Staphylococcus aureus (MRSA) Late-onset pneumonia is due to P aeruginosa, Acinetobacter, or MRSA in 30 to 71% of cases.
Physiotherapy and Other Management[edit | edit source]
Other health professionals will be treating your patient. What is their input?When addressing HAP, respiratory physiotherapy interventions should be individually tailored around the patient’s symptoms, observing aspects such as degree of pain, mobility capabilities and an array of complex factors[13]. Therefore techniques may include positional manipulations (addressing V/A matching and attempting to uses gravity to potentially enable drainage), manual hyperinflation, percussion, shaking, vibrations, suctioning (if huffing or cough promoting techniques are proving ineffective in regards to sputum extraction), breathing exercises including thoracic expansion and relaxing tidal volumes, while also engaging sputum reduction through active cycle and autogenic drainage techniques) as well as mobilization[13]. The later of course demonstrating great importance not only in terms of improving the patients’ respiratory distress, but also in reducing overall hospitalization.
Published substantial evidence very much supports the role of physiotherapy in the respiratory managing HAF, demonstrating both short-term and longer term benefits[13]. However, its essential to promote physiotherapy treatment as part of a multi-disciplinary approach as aspects including pharmaceutical interventions play an integral part in controlling bacterial diseases, promoting lung function and reducing problematic symptoms[14].
Prognosis[edit | edit source]
HAP is linked with increased death rates. The death rates associated with VAP ranges from 20% to 50% in different studies.[12]
Prevention[edit | edit source]
Several basic nursing interventions are associated with reducing HAP risk—
- Following infection prevention standards
- Elevating the head of the bed 30 to 45 degrees to prevent aspiration
- Seeing to good oral hygiene (cleaning teeth, gums, tongue, dentures)
- Increasing patient mobility with ambulation to eg three times a day (as appropriate)
- Educating patient re coughing and deep breathing, and use of incentive spirometry.[2]
For more see Infection Prevention and Control
References[edit | edit source]
- ↑ NICE Hospital-acquired pneumonia caused by methicillin-resistant Staphylococcus aureus: telavancin Available:http://www.nice.org.uk/advice/esnm44/chapter/full-evidence-summary (accessed 25.12.2022)
- ↑ 2.0 2.1 American Nurse Preventing hospital-acquired pneumoniaAvailable:https://www.myamericannurse.com/preventing-hospital-acquired-pneumonia/ (accessed 25.12.20220
- ↑ Radiopedia Hospital-acquired pneumonia Available:https://radiopaedia.org/articles/hospital-acquired-pneumonia-1?lang=us (accessed 24.12.2022)
- ↑ Rotstein C, Evans G, Born A, Grossman R, Light RB, Magder S, McTaggart B, Weiss K, Zhanel GG. Clinical practice guidelines for hospital-acquired pneumonia and ventilator-associated pneumonia in adults. Canadian Journal of Infectious Diseases and Medical Microbiology. 2008;19(1):19-53.
- ↑ Osei‐Bimpong, A., R. McLean, E. Bhonda, and S. M. Lewis. "The use of the white cell count and haemoglobin in combination as an effective screen to predict the normality of the full blood count." International journal of laboratory hematology 34, no. 1 (2012): 91-97.
- ↑ 6.0 6.1 6.2 Tracy, Russell P., Rozenn N. Lemaitre, Bruce M. Psaty, Diane G. Ives, Rhobert W. Evans, Mary Cushman, Elaine N. Meilahn, and Lewis H. Kuller. "Relationship of C-reactive protein to risk of cardiovascular disease in the elderly results from the Cardiovascular Health Study and the Rural Health Promotion Project." Arteriosclerosis, thrombosis, and vascular biology 17, no. 6 (1997): 1121-1127.
- ↑ 7.0 7.1 Marcos, M. A., MT Jimenez de Anta, J. P. De La Bellacasa, J. González, E. Martinez, E. Garcia, J. Mensa, A. De Roux, and A. Torres. "Rapid urinary antigen test for diagnosis of pneumococcal community-acquired pneumonia in adults." European Respiratory Journal 21, no. 2 (2003): 209-214.
- ↑ Pugin, Jérôme, Raymond Auckenthaler, Nabil Mili, Jean-Paul Janssens, P. Daniel Lew, and Peter M. Suter. Diagnosis of ventilator-associated pneumonia by bacteriologic analysis of bronchoscopic and nonbronchoscopic blind bronchoalveolar lavage fluid. American Review of Respiratory Disease 143, no. 5_pt_1 (1991): 1121-1129.
- ↑ 9.0 9.1 Musher, Daniel M., Roberto Montoya, and Anna Wanahita. "Diagnostic value of microscopic examination of Gram-stained sputum and sputum cultures in patients with bacteremic pneumococcal pneumonia." Clinical infectious diseases 39, no. 2 (2004): 165-169.
- ↑ 10.0 10.1 Marc A. Rodger, Marc Carrier, Gwynne N. Jones, Pasteur Rasuli, Francois Raymond, Helene Djunaedi, and Philp S. Wells. "Diagnostic Value of Arterial Blood Gas Measurement in Suspected Pulmonary Embolism", American Journal of Respiratory and Critical Care Medicine, Vol. 162, No. 6 (2000), pp. 2105-2108.
- ↑ 11.0 11.1 Blackmore CC, Black WC, Dallas RV, et al. Pleural fluid volume estimation: a chest radiograph prediction rule. Acad Radiol 1996;3:103–9.
- ↑ 12.0 12.1 Shebl E, Gulick PG. Nosocomial Pneumonia. InStatPearls [Internet] 2021 Jul 21. StatPearls Publishing.Available;https://www.ncbi.nlm.nih.gov/books/NBK535441/#!po=22.7273 (accessed 25.12.2022)
- ↑ 13.0 13.1 13.2 Denehy L, Berney S. Physiotherapy in the intensive care unit. Physical Therapy Reviews. 2006;11(1):49.
- ↑ Berney S, Denehy L. A comparison of the effects of manual and ventilator hyperinflation on static lung compliance and sputum production in intubated and ventilated intensive care patients. Physiotherapy Research International. 2002;7(2):100.
