Hospital acquired pneumonia remains an important cause of mortality. It includes healthcare associated pneumonia and ventilator associated pneumonia. The document discusses the definition, epidemiology, etiology, pathogenesis, diagnosis and treatment of hospital acquired pneumonia. Effective preventive strategies and prompt initiation of appropriate antibiotic therapy based on local microbiology patterns are important for management.
Despite modern anti-tuberculous chemotherapy, approximately 2% of all cases of pulmonary mycobacterial infection require surgical treatment.Therefore, surgical treatment of pulmonary mycobacterial disease is rarely necessary.Types of surgical procedures for PTB include: Collapse therapy, pulmonary resection, lung decortication, drainage procedures such as closed tube thoracostomy, rib resection and open window thoracotomy beside pulmonary resection+ collapse therapy (thoracoplasty). The decreasing morbidity and mortality of pulmonary resection for PTB is due to careful patient selection ( failure of chemotherapy, massive haemoptysis, BPF), improved anaesthetic techniques, stapling devices and better chemotherapy.The prognosis after successful resection is excellent ( 90% survive and remain disease free).
Despite modern anti-tuberculous chemotherapy, approximately 2% of all cases of pulmonary mycobacterial infection require surgical treatment.Therefore, surgical treatment of pulmonary mycobacterial disease is rarely necessary.Types of surgical procedures for PTB include: Collapse therapy, pulmonary resection, lung decortication, drainage procedures such as closed tube thoracostomy, rib resection and open window thoracotomy beside pulmonary resection+ collapse therapy (thoracoplasty). The decreasing morbidity and mortality of pulmonary resection for PTB is due to careful patient selection ( failure of chemotherapy, massive haemoptysis, BPF), improved anaesthetic techniques, stapling devices and better chemotherapy.The prognosis after successful resection is excellent ( 90% survive and remain disease free).
Mauritius - History
Mauritius was known to the early Arab traders, as it can be found marked on their maps, but the first visitors from Europe were the Portuguese, who landed in 1510.They used the island as a victualling stop on the ways to Goa and Malacca, but did not settle.
The first attempt at colonisation was made by the Dutch, who arrived in 1598, and named the island Mauritius, after Prince Maurice of Nassau. They introduced sugar, Malagasy slaves, and a herd of Javanese deer.
The Dutch were heedlessly destructive and were responsible for the disappearance of the magnificent ebony forests and the extinction of the Dodo. They eventually abandoned their settlements in 1710.
The French occupied the island between 1715 and 1810, and renamed it Isle de France, and today many place names are reminders of this period. Mahé de Labourdonnais, who took over as governor in 1735, rebuilt Port Louis and opened the first sugar mill.
In 1810, with the British takeover, the name reverted to Mauritius. The abolition of slavery then led to the importation of Indian and Chinese labourers who were followed by traders of same nationalities. Mauritius obtained independence from Britain on 12 March 1968, and since then has been an independent sovereign nation within the commonwealth.Under the Constitution, which is based on the Westminster model, political power is vested in the Prime Minister and the cabinet.
Elections are usually held every five years. Mauritius became a Republic 0n 12 March 1992. Population Mauritius has a population estimated at 1,150226 people, with about 35 663 on Rodrigues island, a small dependency which forms part of Mauritius. The percentage rate of population growth is 1.1 per annum and the density is approximately 578 per square kilometre. Mauritius has a young educated population, which is remarkable for its ethnic diversity with Mauritians of Indian, African, European and Chinese origin. This has produced a brew of languages, religions and customs.
English is the official language but almost everyone speaks French. Oriental languages, especially Bhojpuri, Hindi and Hakka figure prominently but Creole remains the "Lingua Franca".
Mauritius - History
Mauritius was known to the early Arab traders, as it can be found marked on their maps, but the first visitors from Europe were the Portuguese, who landed in 1510.They used the island as a victualling stop on the ways to Goa and Malacca, but did not settle.
The first attempt at colonisation was made by the Dutch, who arrived in 1598, and named the island Mauritius, after Prince Maurice of Nassau. They introduced sugar, Malagasy slaves, and a herd of Javanese deer.
The Dutch were heedlessly destructive and were responsible for the disappearance of the magnificent ebony forests and the extinction of the Dodo. They eventually abandoned their settlements in 1710.
The French occupied the island between 1715 and 1810, and renamed it Isle de France, and today many place names are reminders of this period. Mahé de Labourdonnais, who took over as governor in 1735, rebuilt Port Louis and opened the first sugar mill.
In 1810, with the British takeover, the name reverted to Mauritius. The abolition of slavery then led to the importation of Indian and Chinese labourers who were followed by traders of same nationalities. Mauritius obtained independence from Britain on 12 March 1968, and since then has been an independent sovereign nation within the commonwealth.Under the Constitution, which is based on the Westminster model, political power is vested in the Prime Minister and the cabinet.
Elections are usually held every five years. Mauritius became a Republic 0n 12 March 1992. Population Mauritius has a population estimated at 1,150226 people, with about 35 663 on Rodrigues island, a small dependency which forms part of Mauritius. The percentage rate of population growth is 1.1 per annum and the density is approximately 578 per square kilometre. Mauritius has a young educated population, which is remarkable for its ethnic diversity with Mauritians of Indian, African, European and Chinese origin. This has produced a brew of languages, religions and customs.
English is the official language but almost everyone speaks French. Oriental languages, especially Bhojpuri, Hindi and Hakka figure prominently but Creole remains the "Lingua Franca".
Otitis is one of the most frequent diseases in early childhood and one of the reasons for first prescription of antibiotics.
Most frequently reported pediatric bacterial infection, with up to 85% of children experiencing an episode by the age of 3 years and many of them have to treat with medicine and surgical management is restricted
Definition of Hospital by W.H.O.
History Of Hospital Development.
Factors Responsible For Development Of Hospitals.
Classification of Hospitals.
Function Of Hospitals.
Factor Affecting Distribution Of Beds.
Factors Influencing Hospital Utilization.
Administration.
Role of Administrator.
Management.
Scaler Principle.
Person reporting directly to Administrator.
HAP/VAP 2016 ATS/IDSA Guidelines. Our Data available at: https://rdcu.be/Mx8EDr Sandeep Kumar
Management of Adults With Hospital-acquired and
Ventilator-associated Pneumonia: 2016 Clinical Practice
Guidelines by the Infectious Diseases Society of America
and the American Thoracic Society.
To see our study results on HCAP and HAP, VISIT https://link.springer.com/article/10.1007/s00408-018-0117-7
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
3. Introduction.
• Hospital acquired pneumonia (HAP) remains
important cause of mortality despite of
advance antimicrobial therapy and better
preventive care . May be managed at ward or
icu.
• Ventilator associated pneumonia( VAP )
• Health care associated pneumonia.(HCAP)
4. Definition
• HAP- pneumonia that occurs 48 hours or more after
admission which was not incubating at the time of
admission.
• VAP- pneumonia that arises more than 48-72 after
endotracheal intubation.
• HCAP- pneumonia in a patient who was hospitalised in
acute care setting for two or more days within 90 days
of infection; residing in nursing homeor long term
facility; received recent iv antibiotic;
chemotherapy;wound care within 30 days of current
infection;attended a hospital or haemodylisis centre.
5. Cont..
• Most of the current DATA have collected from
VAP .
• Microbiological data from non intubated
patient is less accurate.
• Data can be applied to all patients of HAP
6. Epidimology
• 5 to 10 per 1000 hospital admission
• 6 -20 fold increased in mechanicaly ventilated
patients
• 25 % ofall ICU infections.
• 90 % of HAP occurs during mechanical
ventilation.
• Incidence of VAP highest in early days of hoispital
admission ( ≤ 5 days ).
• Early onset VAP or HAP (≤ 4 days ).
• Crude mortality rate 30- 50%
7. INCIDENCE IN INDIA :-
• Incidence of HAP in india is 53.9%.
• Incidence of VAP in india is 8.95/1000 ventilator
days.
• Mortality rate(attributable) is 37% - 47.3%
Park Es et al Am j inf control(2000)
8. Etiology
• Mostly wide spectrum of bacterial pathogens
• May be polymicrobial
• Viral or fungal pathogens in
immunocompromosed host.
9. Etiology
• P. areuginosa
• Escherichia coli
• Klebsiella pneumonie aerobic gram negetive
• Acinetobacter sp
• MRSA ( DM, head trauma,haemodylisis ,ICU patients)
• Streptococcus viridans
• Coagulase negetive staph immunocompr
• Fungal
• Viral (seasonal ,influenza A ,parainfluenza,adeno,rsv)
• Anerobic - occurs in non intubated patient following
aspiration,rare in patients with VAP.
10. Etiology for MDR infection
• Infection with multi drug resistant ( M D
R)strain is major concern in treating HAP.
• Frequency of MDR pathogens causing HAP
may vary by hospital ,patients population
,exposure to antibioticatype of ICU patient,
and changes over time, emphasizing the need.
• MRSA , pseudomonas, acinatobacter,
klebsiella are of main concern.
13. Risk factor
• Non modifiable risk factor
I. male sex
II. Preexisting pulmonary disease
III. Multiple organ system failure
14. Modifiable risk factor
• Intubation and mechanical ventilation ( 6-21 %
increasd risk of HAP ).
1. TYPE OF ET TUBE
2. COLONISATION IN VENTILATOR
CIRCUIT
3. USE OF SEDATIVE OR PARALYTTIC
AGENTS
4. CUFF PRESSURE
5. COLONISATION IN PASSIVE
HUMIDIFIER
15. Aspiration ,body position ,enteral feeding
• Supine position
• Enteral feeding a risk factor ..?
• Colonisation of pathogen in oral cavity
• stress ulcer prophylaxis with H2 blocker.
• Blood transfusion .
• Hypo and hyper glycaemia.
16. - PREVENTIVE STRATEGIES FOR NOSOCOMIAL
PNEUMONIA :
1) Implementation ,as VAP bundle,of noso-
comial pneumonia preventive strategies
that have proven efficacy in reducing mo-
rbidity & mortality.
17. 2) Implementation of education programmes
(respiratory care physicians & nurses being
primary recepients),& frequent performance
feedbacks & compliance assesment.
3) Strict alcohol based hand hygiene.
4) Avoidance of tracheal intubation & use of NIV
when indicated(acute exacebn. of COPD,
acute hypoxemic resp failure,immunocomp.
with pulmonary infiltrates)
-Recent reports emphasize role of NIV in
preventing re-intubation in recently extubated
pts at risk for relapse & respiratory failure.
18. 5) Daily sedation vacation & implementation of weaning
protocols.
6) No ventilatory circuit tube changes unless soiled or
damaged.
7) Use of tracheal tubes with cuff made of novel
materials(polyurethane; & LVLP cuffs made of silicone
&latex) & shape(conical)
8)Application of low level PEEP(5-8cm H2O)during
tracheal intubation.
9) Use of silver coated ETT –
NASCENT trial concluded that silver coated
ETT has ↓ incidence of VAP,↓ mortality in pts
with VAP,is cost effective & has greatest
impact during first 10 days.
19. 10) Aspiration of subglottic secretions(every 4-6hrs)
11) Internal cuff pressure maintained within 25-30
cm H2O & carefully controlled during transport
of patients outside ICU.
12) Earlier tracheostomised pts (mean~7 days)
had shorter length of M/V & ICU stay,a ↓trend
towards pneumonia but no survival benefit as
compared to late tracheostomy(mean~14 days)
13) Routine saline instillation before tracheal
suctioning not recommended
20. 14) Intubated pts should be kept in semi-recumbent
position(30-45°),rather than supine to prevent
aspiration;especially when enterally fed.
15) Continuous lateral rotation of bed helps to reduce
extravascular lung water,improveV/Q
& enhance mobilization of secretions.
16) Post pyloric feeding in patients with impaired
gastric emptying
17) Risk of VAP associated with early enteral feeding
didn`t translate into ↑ risk of death,so,early enteral
feeding advised.
21. 18) Stress ulcer prophylaxis in high risk pts(coagulopathy,↑
duration of M/V,h/o
GI bleed.
19) Oral care with 2% chlorhexidine.
20) SELECTIVE CONTANINATION OF DIGESTIVE TRACT (SDD) :
- consists of nonabsorbable antibio. Against
gram – (tobramycin.polymyxin E) + nystatin/
ampho B for candida administered into GI to
prevent oropharyngeal & gastric colonization.
- SDD reduces incidence of VAP & it’s the only
strategy that has shown survival benefit
22. • Blood sugar controll 80-110mg
• Decision of blood transfusion should defered
till hb% less than 7gm% instead of 9 gm%.
23.
24. Pathogenesis
• Shifting of delicate balance of host defence vs
colonisation and invasion in favour of
pathogens to persist and invade in lower
respiratory tract.
25. Pathogenesis
entry of microbial pathogens in LRT
colonisation
overcome the host mechanical ( cilia,mucus)
humoral ( antibody ,complement) , cellular
(PMN,macrophages, lymphocytes)
infection
26. Pathogenesis
• Source of pathogens include environment, transfer of
microbes.
• Colonisation fsvouring factor( prior surgery ,ivasive
respiratory device, immuno deficient state,prolong
antibiotic therapy)
• Aspiration f oropharyngeal pathogens ,leaking around ET
tube,.
• Direct inoculation of pathogens into lower
airway,haematogenous spread from infected catheter ,
microbial translocation from GI lumen.
• Infected biofilm in the ET tube.
• Stomach and sinus may act as potential reservior of
nosocomial pathogen by favouring colonisation.
27.
28. Diagnosis
• To confirm the diagnosis of pneumonia.
• To identify the causative agent for pneumonia.
29. • - NON INFECTIOUS CAUSES OF
FEVER/INFILTRATES MIMICKING NOSOCOMIAL
PNEUMONIA :
- chemical pneumonitis
- atelectasis
- pulm embolism
- ARDS
- pulmomary hemorrhage
- lung contusion
- infiltrative tumour
- radiation pneumonitis
- drug reaction
- BOOP
30. Suspicion of HAP
• suspicion of HAP if fever ,purulent secretion
,leukocytosis,radiological infiltration in chest
xray.
• Tracheo bronchitis is associatd with negetive
xray finding.
• Unexplained haemodynamic instability or
deterioration of blood gases in ventilated
patient.
31. Diagnosis
• Confirmation of diagnosis with identifying the
causetive agent is very challenging.
• Main aim is to differentiated from colonisation
with infection.
• Etiological dignosis requires lower respiratory
secreation culture including endotracheal
aspirate, PSB (protracted brushing), BAL .
• Blood or pleural fluid culture.
32. Diagnosis
• Positive culture cannot always differentiate
from colonisation with infection.
• A sterile culture of LRTI of an intubated
patient in absent of recent change in antibiotic
is strong predictor of absence of pneumonia.(
negetive predictive value).
33. Recommendation for diagnosis
• All patient should undergo detailed clinical evaluation (
history and physical examination).
• Chest radiograph.
• Purulent tracheobroncitis should be properly
diagnosed ( negetive cxr finding)
• All routine blood investigation including ABG should be
done ( severity of ill ness and indicates other organ
involvement,need for oxygen)
• Blood culture and pleural fluid culture should be done.
• Samples of LRT should obtain in all suspected case of
HAP and should collected before antibiotic changes.
34. Recommendation for diagnosis
• Absence of clinical suspicion of HAP of TAB no
further workup necessary
• Sterile culture with no change of antibiotic
negetive for bacterial pneumonia but viral or
legionella pneumonia may presesnt.
• Search for extrapulmonary infection according
to clinical suspicion.
35. Diagnostic Strategy
• Clinical suspicion is over sensitive further
diagnostic approach needed for optimal
management.
• To ensure collection of appropiate sample.
• To promote use of early and effective
antibiotic therapy.
• Streamlinig or de esclation when possible.
• To identify extra pulmonary infections.
37. Clinical strategy
• Pneumonia = infiltrate in xray+ Two among three clinical criteria ( fever> 38
,leukocytosis or leukopaenia and purulent secretion) .
• Etiological cause is defined by semiquantative culture (light, moderate ,heavy) of
endo tracheal aspirate or sputum with initial microscopic examination.
• CPIS score used to increase accuracy in clinical strategy. CPIS > 6 then good co
relation with pneumonia.
• Intial gram stain to star empirical antibiotic therapy.
• Reevaluation of decision of using antibiotics done based on result of
semiquantetive culture report by day 3 or sooner
38. Bacteriological strategy
• Quantitative culture for lower respiratory tract done to
define presence of pneumonia and etiological
pathogen.
• Growth above thresold concentration required to
diagnose VAP/HAP
• Target is to avoid overtreatment antibiotic therapy
• Major concern is false negetive report may be lead to
failure to treat a specific pathogen .false negetive
reporty may be due to prior antibiot therapy.
• Endotracheal aspirate collected bronchoscopicaly and
non bronchoscopicaly and each technique has its
diagnostic threshold and methodological limitation
39. • CLINICAL PULMONARY INFECTION SCORE (CPIS) :
criterion 0 1 2
tracheal secn . (-) not purulent purulent
x- ray infiltrates NO DIFFUSE LOCALISED
temp °C ≥36.5&≤38.4 ≥38.5&≤38.9 ≥39or≤36
leucocytes ≥4000&≤11000 <4000or>11000 +immature
neutrophil >50%
microbio (-) (+)
40.
41. Dignosis strategy final..
• Patient with suspected VAP LRT sample should sent for
culture and extra pulmonary infection should be
excluded before starting antibiotic therapy.
• If there high pre test probability and with sepsis
prompt therapy should started immidiately .
• Bronchoscopy sampling prefered if not available then
non bronchoscopic sampling to be done and
quantitavie culture should be priority over
semiquantitavie culture.
• Therapy should not be postponed for purpose of
diagnosis.
42. • isolation of candida albicans and other cadida
species in bronchoscopy is very common
mostly due to colonisationrather
pneumonia,and usuly no treatment is
required.
• Diagnosis of viral infection made by rapid
antigen testing and viral culture or serological
assays.
46. Treatment
• Initial concern should be etiological pathogen
MDR or not.
• Evaluation of risk factor for MDR pathogen.
• Prompt initiation of therapy.
• Patient with HCAP considerd to be infected
with MDR.
49. Treatment
• Choice of specific agent should dictated by local
microbiology,cost ,availability ,and formulatory restriction.
• Altarnate group of antibiotic should be selected if patient
received recent antibiotic therapy .
• On admission iv antibiotic therapy should be started .
• Combination therapy should be done if patients likely to
infected with MDR pathogens. Role is doubtful in comparison
to monotherapy except to enhance the likelyhood of initially
appropriate empiric therapy.
50. • Aminoglycosides can be stopped after 5-7 days if used with
combined therapy in a responding patients.
• Patient withh risk group should initialy receive combination
therapy until result of culture confirms that single agent can
be used
• If etiological agent is not p.aruginosa patient is having a good
response to intial antibiotic therapy , duration can be
shortened to 7 days in comparison to traditional 14 to 21 days
51.
52.
53. Important notes for specific pathogens
doccumented Pathogens Therapy recomendation
P aeruginosa Combined therapy. to avoid resistence (
weak evidence). Mojor concern is to avoid
inappropriate and ineffective treatment.
Acinetobacter spp. Carbapenem, sulbactum ,colistin, and
polymixin. No doccumented benefit in
combined therapy.
ESBL enterobacteriaceae Monotherapy with third generation
cephslosporin avoioded most active
MDR Gram negetive pneumonia
Not improving with systemic therapy
Adjunct therapy with inhaled
aminoglycoside or polymixin B.
Linezolid is an alternative to vancomycin for the treatment of MRSA VAP.
54. Response to therapy
• Clinical improvement usually takes 48-72 hours. Therapy
should not be changed during this window unless rapid
clinical decline.
• Non response to therapy usually evident on DAY 3 by
asesing clinical parameter.
• Serial respiratory tract culture can be used for defining
resolution , superinfections , recurrent infection or
microbiological persistense
• Chest radiography has limited value ,initial radiographic
deterioration is very much common.rapid deterioration or
multilobular involvement > 50% increase in size of lesion
,development of cavity ,significant pleural effusion, should
raise concern.
55. • WBC count, measures of oxygenation ,core
temperatue have used in several studies to
define normal pattern of resolution
• CPIS scoring can be used to predict resolution
at 3 days.
56. Reasons of non resolution
• Wrong diagnosis.
• Extrapulmonary infection not evluated.( UTI ,catheter
related infection,sinusitis,pseudomembrenos colitis.
• Resistant pathogen.
• Development of complication (lung abcess,empyema)
• complication during treatment.Drug fever ,sepsis with
MODS, pulmonary embolus with secondary infraction.
• Unusual pathogen not considered in emperical
therapy( m.tuberculosis ).
• Unrecognised immunosuppression , unrecognised
pneumocystis carini infection.