Hospital Acquired Pneumonia

Definition/Description

Distinguishing between pneumonia and Hospital-acquired pneumonia


Pneumonia

“Pneumonia is an infection of the lung tissue. When a person has pneumonia the air sacs in their lungs become filled with microorganisms, fluid and inflammatory cells and their lungs are not able to work properly. Diagnosis of pneumonia is based on symptoms and signs of an acute lower respiratory tract infection, and can be confirmed by a chest X-ray showing new shadowing that is not due to any other cause (such as pulmonary oedema or infarction)." [1]
(NICE clinical guidelines 2014)


Hospital-acquired pneumonia

"Hospital-acquired pneumonia 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) hospital-acquired pneumonia 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) hospital-acquired pneumonia 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."[2]

(NICE Guidelines. Published: 15 July 2014)


Epidemiology

“At any time 1.5% of hospital inpatients in England have a hospital-acquired respiratory infection, more than half of which are hospital-acquired pneumonia and are not associated with intubation. Hospital-acquired pneumonia is estimated to increase hospital stay by about 8 days and has a reported mortality rate that ranges from 30–70%. Variations in clinical management and outcome occur across the UK.”[1]

(NICE guidelines 2014)


Ventilator-acquired pneumonia (VAP) has been studied more comprehensively than HAP. A clear reason for this is VAP is responsible for 86% of the HAP reported[3].

The incidence rate of HAP is between 3 and 10 per 1000 hospital admissions[4][5].


Mortality rates from VAP are between 24 and 50% but it is reported to jump to 76% if it is caused my multi drug resistant pathogens that are often linked to later stage pneumonia (> 5days in hospital)[3]. Although it is difficult to determine the exact cause of death in critically ill patients, which will cause discrepancies in any date, Accurate antibiotics taken at the right time has shows to lower mortality rate for HAP.


The chance of infection is estimated to be 3%/day during the first 5 days of ventilation, followed by 2%/day up to day 10 of ventilation and there- after 1%/day.[6]



Aetiology

The most common cause is an accumulation of bacteria, most ordinarily gram-negative bacilli and staphlycoccus aureus, which inhabit the oropharynx and upper airways in seriously ill and ventilated patients[7]. A less common cause is seeding of the lung due to bacteremia; a bacterium that originates in the patients’ blood supply and can transferred to the lungs during gas exchange. Finally inhalation of bacterially contaminated aerosols which transport airborne particles containing Legionella sp, Aspergillus sp, or influenza virus, although this is a relatively unfamiliar form of contracting hospitalized pneumonia[7].


Endotracheal intubation with mechanical ventilation poses the greatest overall risk[8]. Ventilation Associated Pneumonia is a subcategory of hospitalized and contributes more than 85% of all cases, with pneumonia occurring in up to 27% of ventilated patients[8]. Endotracheal intubation related bacteria embed themselves deep into the endotracheal tube cuff enabling them to avoid the body' nature immune response while also providing a biofilm of protection from antibiotics[7].


In non-intubated patients, risk factors include previous antibiotic treatment, high gastric pH, resulting from cardiac, pulmonary, hepatic, or renal deficiencies[7]. Major risk factors for postoperative pneumonia are patients older than 70, abdominal or thoracic surgery, and cardiorespiratory functional depletion[7].

Investigations

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[9].
CRP (to aid diagnosis and as a baseline measure). The C-reactive protein (CRP) test is a diagnostic tool that identifies regions of inflammation[10]. 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[10]. The CRP test can be used in adjunction with signs, symptoms and other tests in order to fully evaluate patients with HAP[10].


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[11]. 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[11].


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[12].


Sputum examination and culture.
Sputum Examination is a diagnostic tool used to identify bacteria and fungi located in the pulmonary facet[13]. 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[13].


Blood gases:
Blood gases will demonstrate how well both the respiratory and the renal systems are functioning[14]. 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[14].


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[15]. Samples of the pleural fluid are sent for analysis which includes cytology for malignant cells and bacteriology for identification of foreign bacteria[15].

Clinical Manifestations

A patient that develops new or extra pulmonary infiltrates and a fever are signs of HAP. In order to differentiate HAP and other pathologies diagnosis should be based on a radiographic x-ray. To diagnose HAP radiological opacity with alveolar condensation must be present.[16]


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

Physiotherapy and other management. 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[17]. 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[17]. 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[17]. 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[18].

Prevention

Three European societies, (European Respiratory Society (ERS), European, Society of Clinical Microbiology and Infectious Diseases (ESCMID) and European Society of Intensive Care Medicine (ESICM), in 2008 produced a report to further the clinical guidelines of HAP and VAP. Within these guidelines they outline several measures that can have proven to reduce the likelihood of HAP.

Generally recommended general measures:

  • Alcohol-based hand disinfection
  • Use of microbiologic surveillance
  • Monitoring and early removal of invasive devices
  • Programs to reduce antimicrobial prescriptions
  • Generally recommended specific measures
  • Avoidance of endotracheal intubation
  • Avoidance of reintubation
  • Preference of noninvasive ventilation (NIV)
  • Preference of orotracheal intubation and orogastric tubes
  • Maintenance of the ET cuff pressure at approximately 20 cmH2O
  • Avoidance of flushing the condensate into the lower airway or to in-line medication nebulizers Patient positioning (semirecumbent position)[19]


Additional measures which might be helpful in distinct settings and populations:

  • Continuous aspiration of subglottic secretions
  • Endotracheal tubes coated with antiseptics or silver
  • Preference of heat-moisture exchangers (HMEs) over heater humidifiers (HH)
  • Oral decontamination
  • Selective decontamination of the digestive tract (SDD)[19]


The VAP Guidelines Committee and the Canadian Critical Care Trials group in 2008 recommended several approaches to encourage a reduction in incidences[20]:

  • The orotracheal route of intubation should be used when intubation is necessary
  • There should be no scheduled ventilator circuit changes but new circuits for each patient, and changes if the circuits become soiled or damaged
  • Changes of heat and moisture exchangers with each patient, also every 5-7 days and as clinically indicated
  • Closed endotracheal suctioning system, and that the system is changed for each patient and as clinically indicated.
  • The use of subglottic secretion drainage in patients expected to be mechanically ventilated for > 72hrs
  • Bed head to be elevated to 45°. If this angle is not possible then as much elevation as possible is recommended
  • The use of oral antiseptic chlorhexidine
  • The use of oral antiseptic povidone-iodione should be considered with patients with severe head injury
  • Rotating beds should be considered


Resources

NHS website
http://www.nhs.uk/conditions/pneumonia/Pages/Introduction.aspx

Patient website
http://www.patient.co.uk/health/pneumonia-leaflet

Recent Related Research (from Pubmed)

References

see adding references tutorial.

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