Presentation on theme: "Yong Lee ICU Registrar John Hunter Hospital"— Presentation transcript:
1 Yong Lee ICU Registrar John Hunter Hospital PneumoniaYong LeeICU RegistrarJohn Hunter Hospital
2 Objectives Pathogenesis Pathophysiology Clinical features Community acquired pneumonia, investigations, assessments of severity, empirical therapyMRSA InfluenzaNosocomial pneumonia
3 Pathogenesis 3 major routes of entry Upper airway colonisation Oropharyngeal or gastric aspiration *Inhalation of aerosolsHaematogenousUpper airway colonisationS.Pneumoniae, H. Influenzae, Mixed aerobic and anaerobic bacteriaE.Coli, Klebsiella more frequent in alcoholics, institutionalised elderly, poor oral hygieneNormal host defensesBronchial mucociliary clearance, phagocytic cells in alveoli and bronchial mucosa
4 Quantity of material aspirated Uncontrolled seizures, abnormal airway motor control periodontal disease, bronchial obstructionNature of bacteria in aspirated materialHighly efficient pathogens (legionella, mycoplasma, chlamydia, coxiella, fungal)Efficiency of host’s pulmonary defense mechanismsPost viral respiratory infection, alcoholics, COPD with impaired mucociliary clearance, relative immunologic impairmentHaematogenous spreadEstablished infection elsewhere (IV drug user)From damaged skin (brucellosis, melioidosis)
5 PathophysiologyProliferation of microorganisms within pulmonary parenchyma elicit host’s acute inflammatory responseExudation of protein rich fluid and phagocytic cellsLocal mechanical consequencesImpaired distribution of ventilation, decrease in lung compliance -> dyspnoeaV/Q mismatchSystemic changesActivation of acute inflammatory response (interleukin 1, cytokines) result in fever, leukocytosisBacteremia or microbial antigenemia may activate systemic inflammatory response leading to septic shock
6 Clinical features Systemic response Pulmonary symptoms Physical Fever, increased WCC, other sepsis syndromesPulmonary symptomsCough, sputum production, dyspnoea, pleuritic chest painPhysicalInflammatory pulmonary parenchymal process (rales, tachypnoea)Consolidation (bronchial breathing, dullness to percussionAbnormal lung function (arterial hypoxaemia, hypocapnia)Radiographic pulmonary infiltrate c/w pneumonia
9 Assessment Clinical features c/w pneumonia Consider patient’s age and co-morbiditiesThe presence of clinical features of organ system failuresCXR demonstrating consolidationConsider mild (outpatient with appropriate follow up), moderate or severeInvestigation for causal pathogenSputum gram stain*, blood culturesPneumococcal and legionella urinary antigen assay, nose and throat swab for respiratory viral nucleic acid testing (PCR)Mycoplasma IgM serology, acute and convalescent serology for mycoplasma, legionella, chlamydophilia and influenzaProcalcitonin**BAL
10 Assessment of severity PSI (Pneumonia Severity Index)CURB 65 (Confusion, Urea, Resp rate, Blood pressure, age <65)Both developed from statistical analyses of features c/w 30 mortalityHowever majority of patients who die of CAP are elderly persons with multiple co-morbidityTools predicting mortality are less accurate in identifying patients who will benefit from admission to ICUCORBSMART-COP
11 CORB C = acute confusion O = oxygen saturation 90% or less R = respiratory rate 30 breaths or more per minuteB = systolic blood pressure less than 90 mm Hg or diastolic blood pressure 60 mm Hg or lessInterpretation of CORB score'Severe CAP' = the presence of at least two of these features.In the Australian study cohort, the accuracy of CORB for predicting need for IRVS using presence of at least two features was:sensitivity = 81%, specificity = 68%positive predictive value (PPV) = 18%negative predictive value (NPV) = 98%area under the receiver operating characteristic (ROC) curve = 0.74.
13 SMART-COP Interpretation of SMART-COP score 0 to 2 points—low risk of needing intensive respiratory or vasopressor support (IRVS)3 to 4 points—moderate risk (1 in 8) of needing IRVS5 to 6 points—high risk (1 in 3) of needing IRVS7 or more points—very high risk (2 in 3) of needing IRVSSevere CAP = a SMART-COP score of 5 or more points.In the Australian Community-Acquired Pneumonia Study (ACAPS) cohort, the accuracy for predicting receipt of IRVS with a SMART-COP score of 3 or more points was:sensitivity = 92%specificity = 62%PPV = 22%NPV = 99%area under ROC curve = 0.87.The SMART-COP severity scoring tool can be modified to make it suitable for use by primary care physiciansA modified version has also been developed for use in tropical Australia
14 Empirical management Mild CAP If no improvement in 48 hrs Reasonable for single shot benzylpenicillin 1.2gAmoxycillin 5 – 7 daysOr if atypical is suspectedDoxycycline or Clarithromycin (as single agents)If no improvement in 48 hrsConsider dual therapy of amoxycillin + doxycycline or clarithromycinSome resistant strains of doxycycline and clarithromycin streptococcus pneumoniae in some regions, consider switching to cefuroxime or moxifloxacin or assess need for hospital admission
15 Empirical management Moderate CAP Tropical or non tropical region, risk factors for Burholderia pseudomallei, Acinetobacter baumannei (DM, chronic lung disease, heavy ETOH, chronic renal failure)Non tropical, no risk factorsBenzylpenicillin IV PLUS Doxycycline/ Clarithromycin OralAdd Gentamicin or change to ceftrixone if GN Bacilli identifiedTropical, risk factorsCeftriaxone PLUS initial dose of Gentamicin
16 Empirical management Severe Pneumonia Non tropical region Ceftriaxone IVBenzylpenicillin IV + Gentamicin*(short term empirical or directed therapy only)Cefotaxime IVPLUS Azithromycin IV in all casesTropical regionMeropenem IV or Imipenem IVPLUS Azithromycin IV in call cases
17 Staphylococcal pneumonia Clinical presentation is suggestive of staphylococcal pneumoniaR sided endocarditis, IVDU, gram stain positive cluster, CXR with cavitatory pneumoniacMRSA (different from hMRSA)Increasing esp. in indigenous and pacific islander, IVDUMore clinically aggressive but may be susceptible to routine Abx (clindamycin and bactrim)Appropriate susceptibility testing is therefore crucialHospitalised patientsIntubated patients and late-onset nosocomial infectionsSeverely ill patients should be treated for BOTH non-MRSA and MRSA (e.g flucloxacillin & Vancomycin) until susceptibility results available
18 Non MRSA MRSA Flucloxacillin IV Cephalothin or cephazolin IV (if penicillin hypersensitive)Vancomycin (if immediate penicillin hypersensitive)MRSAVancomycin IV*Linezolid, if VISA or hVISAConsider additional if severe (clindamycin, linezolid, rifampicin + fusidic acid) depending on susceptibility
19 Influenza Influenza A and B viruses Usually cause seasonal minor or major epidemicsNovel strains (e.g H5N1, H1N1) also with potential to cause epidemics due to lack of pre-existing immuniity in humansInfection is spread by droplets and fomite contact so appropriate infection control are importantRapid specific testing such as nucleic acid tests (eg polymerase chain reaction [PCR]) for influenza on nose or throat swab specimens are the most useful tests to make the diagnosisClinical features alone may be reliable enough for diagnosis when the pre-test probability of influenza is high, for example during known epidemics.
20 TreatmentTreatment with a neuraminidase inhibitor (oseltamivir or zanamivir) has been associated with a reduced rate of complications of influenza in observational studiesObservational studies have also shown an increase in mortality if hospitalised patients retrospectively shown to have had influenza were not treated with oseltamivir.Treatment is generally thought to be of greatest benefit if commenced early (ideally within 48 hours of symptom onset), and if targeted to people at highest risk of complications.Where severe illness (eg pneumonitis) is already present, treatment should be offered regardless of the patient's risk group or duration of symptomsTreatment should be prioritised for people with risk factors for poor outcomes. For these people treatment may be considered even if commenced more than 48 hours after the onset of symptoms.
21 Treatment High risk groups If treatment indicated Pregnant women, morbidly obese, underlying chronic disease, immunosuppressed, homeless, nursing home residents, indigenous Australians, the elderly and very youngIf treatment indicatedOseltamivir oral for 5 days ORZanamivir inhalation for 5 daysAntibacterials if clinical presentation suggests bacterial or secondary bacterial infection developsVaccination with current influenza vaccine provides protection and complications in ~70% of those vaccinatedRecommended for all health care worker, age >65, Aboriginal/ TSI > 15yProphylaxis should be considered for close contacts of proven cases, particularly if those contacts are themselves in high-risk groups
22 Nocosomial Pneumonia or Hospital Acquired Pneumonia HAP Presentation often unusual because it is affected by advanced age, co-morbidity and neurological disordersClassic respiratory symptoms often mild and extrapulmonary manifestations (e.g. GI disorder, confusion) are frequenyPneumonia that is not incubating at time of admission to hospital and develops in patients hospitalised for 48 h or longerVAP is usually defined as pneumonia developing ≥48 h after implementing ET intubation and/or mechanical ventilation that was not present before intubationDivided to early or late onset
23 Early onset HAP Late onset HAP Within 4 -5 days of hospital admission and tends to be caused by antibiotic sensitive community acquired pathogensHowever, increasing frequency of early onset HAP caused by nosocomial pathogens (? Related to concept of healthcare – associated pneumonia)HCAP - any patient admitted to an acute care hospital for 2 or more days within 90 days of the infection; nursing home resident; attended a hospital or haemodialysis clinic; received recent intravenous antibiotic therapy, chemotherapy, or wound care within the past 30 days of the current infectionLate onset HAPTends to be caused by antibiotic resistant hospital opportunists (e.g. Pseudomonas, MRSA)
24 Diagnosis of HAP Reliable diagnosis is hard If one or more of the following criteria are present, pneumonia should be considered in the differential diagnosis:purulent sputum or tracheal secretions, and new and/or persistent infiltrate on chest X-ray, which is otherwise unexplainedincreased oxygen requirementtemperature greater than 38.3 ºCblood leucocytosis (greater than 11 x 109/L) or leucopenia (less than 4 x 109/L)The presence of bacteria in expectorated sputum or ETT aspirate usually represent colonisation only, and on its own does not justify a diagnosis of HAP
25 HAP aetiologyHospitalised patients frequently develop colonisation of the oropharynx with aerobic GN bacilli, and may also be exposed to multiresistant hospital pathogens e.g.(MRSA), drug-resistant Enterobacteriaceae, Pseudomonas aeruginosa, Acinetobacter species and Stenotrophomonas maltophiliaRecent antibiotic therapy is a distinct risk factor for HAP due to drug-resistant bacteria and/or Pseudomonas aeruginosaIn cases admitted to intensive care for pneumonia management, also consider testing for Legionella (in adults) and influenza infection.
26 HAP Treatment Treatment stratification Low risk of MDR (Low risk ward, high risk area of < 5 days)High risk of MDR (High risk ward >5 days, consider HCAP)Antibiotic susceptibility will differ between institutionsRecommended initial antibiotic regimen may need to cover local pathogens and take account of the patient’s recent Abx exposure and culture resultsFailure to control infection should prompt re-evaluation of antibiotic therapy and consideration of non-infectious diagnoses
27 Low risk MDRO Mild disease Moderate to severe disease Amoxycillin with clavulanic acid oral ORBenzylpenicillin + single dose gentamicinModerate to severe diseaseCeftriaxone IV ORBenzylpenicillin + Gentamicin ORCefotaxime IVTazocin IVTimentin IVAntibiotic susceptibility to guide ongoing therapySwitch to oral Abx after significant improvementConsider early cessation of therapy in patients who are shown to have alternative diagnosis
28 High risk MDR organism Little evidence Tazocin IV or Timentin IV or Cefepime IVIf ventilated patient, add Gentamicin for 1 dose and determine subsequent 1 or 2 doses dependant of renal functionIf predominant GPC (clusters) on gram stain or known to be colonisedVancomycin IVConsider risk factors and extrapulmonary symptoms consider Legionella’sThere is evidence that the response to appropriate ABx Rx for ventilated patients occurs within the first 6 days and that prolonged therapy results in colonisation and re-infection with resistant organisms. Treatment for 8 days is recommended except for Pseudomonas aeruginosa or Acinetobacter species when treatment may be needed for up to 15 days.
29 ReferencesPrinciples of Critical Care 3rd ed. - J. Hall, G. Schmidt, L. Wood (eds) (Mc-Graw-Hill, 2005)Therapeutic guidelines, Antibiotics, 2010Buising KL, Thursky KA, Black JF, MacGregor L, Street AC, Kennedy MP, et al. Identifying severe community-acquired pneumonia in the emergency department: a simple clinical prediction tool. Emerg Med Australas 2007;19(5):418-26Charles PG, Wolfe R, Whitby M, Fine MJ, Fuller AJ, Stirling R, et al. SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clin Infect Dis 2008;47(3):375-84Davis JS, Cross GB, Charles PG, Currie BJ, Anstey NM, Cheng AC. Pneumonia risk stratification in tropical Australia: does the SMART-COP score apply? Med J Aust;192(3):133-6Charles PGP, Whitby M, Fuller AJ, Stirling R, Wright AA, Korman TM, et al, the ACAPS Collaboration, Grayson ML. The eitiology of community-acquired pneumonia in Australia: why penicillin plus doxycycline or a macrolide is the most appropriate therapy. Clin Infect Dis 2008; 46: